'Two as Good as a Hundred':  Poorly Replicated Evidence in Some 19th Century Neuroscientific Research
Forthcoming, Studies in the History and Philosophy of Biology and Medical Science
James Bogen, 
Center for Philosophy of Science, 817 Cathedral of Learning, University of Pittsburgh, Pittsburgh, Pennsylvania, 15206.  jbogen@pitt.edu

No one feels more than I do the difficulty of observing convulsive seizures with sufficient precision for anatomical and physiological uses, and the difficulty there is in defining at autopsies the exact parts of the brain damaged.  The damage by disease is often coarse, ill defined, and widespread.  The facts I have up to this time obtained toward the 'Localization of Movements in the Brain' of man by observing cases are I admit very few, and of a most general character…Nevertheless, I repeat the experiments of disease must be considered in the case of man.(Jackson[1958 I], p.40) 
	i.	Introductory.  John Hughlings Jackson studied epileptics and aphasics from 1861 to 1863 as a reporter for the Medical Times and Gazette and from then on to the end of the century as  a physician in the National Hospital for the Paralyzed and the Epileptic in Queens Square, London.  One of many scientifically and historically important aspects of his work was his use of clinical and post-mortem data to develop what turned out to be an influential and progressive picture of the organization of the brain and its functions. I'll refer to this picture as 'Jackson's Hierarchy', 'JH' for short.
   The subject Jackson investigated was so difficult, and the theoretical and technological means available for its study were so poorly developed that his theorizing was inevitably incomplete and flawed in detail.   But even so, its leading ideas were so fruitful that Otfrid Foerster could say decades later that
[t]he map of the human motor cortex to be found nowadays in every textbook of neurology is nothing else but a copy of the picture engraved in Hughlings Jackson's brain.  (Finger[1994]p.193).
Present day neuroscientists not only agree with Foerster on Jackson's importance, but also give additional reasons for doing so.   
   Jackson's work raises a number of philosophical issues.   The one this paper is concerned with is epistemological.  In developing and confirming his theory Jackson had to rely on sparse and poorly replicated clinical and pathological observations.  But according to a doctrine which philosophers, historians, and sociologists of science tend to accept without question, unreplicated evidence is  epistemically defective.  If the received doctrine is correct, the wide acceptance of JH by the best neuro-anatomists and physiologists among his contemporaries and successors is puzzling.  
   This paper's leading idea is that the received doctrine about the importance of replication is incorrect.  I will illustrate its incorrectness from examples of Jackson's evidence and his use of it.  I hope that apart from the epistemological lessons these examples teach, setting these examples out briefly and systematically will be of some interest to historians.  My versions of Jackson's arguments are rational reconstructions of reasoning whose details must be gleaned from different texts.  The need for this will be apparent to anyone who has read Jackson's papers.  Although they depart drastically in style from Jackson's own presentations, I believe my reconstructions are faithful to their logic
	ii.	The received doctrine about replicability.  The received doctrine about replicability has as a philosophical component the normative claim that only replicable observations of empirically determined effects qualify as epistemically legitimate evidence for or against scientific claims.  Appeals to observations which are not or cannot be well replicated may be rhetorically effective, and may have some significant sociological or psychological influence on the acceptance or rejection of a scientific hypothesis.  But according to the received doctrine they do not confer any rational force upon the arguments in which they occur.  Thus Popper believed that for physics at least 
	1.	Regularity:
Only when certain events recur in accordance with rules or regularities, as is the case with repeatable experiments, can our observations be tested--in principle--by anyone.  We do not take even our own 	observations quite seriously, or accept them as scientific observations until we have repeated and tested them.  Only by such repetitions can we convince ourselves that we are not dealing with a mere isolated 'coincidence', but with events which, on account of their regularity and reproducibility, are in principle intersubjectively testable.(Popper[1959] p.46)	
Popper's requirement for repeatability was a strong one:
	2.		Repeatability: 
..the scientifically significant physical effect may be defined	as that which can be regularly reproduced by anyone who carries out the appropriate experiment in the way prescribed.(ibid)
As will be seen, the application of Popper's requirement to Jackson's evidence would require us to dismiss his arguments for JH out of hand.
   The received doctrine has as a historical component the claim that at least since the 17th century, working scientists have been unwilling to accept or reject substantial theoretical claims on the basis of unreplicable or poorly replicated empirical evidence.  For example, Harry Collins (who is so far from being a Popperian that his agreement with Popper on the importance of replicability is remarkable) said: 
From the scientist's point of view, the establishment of a conceptual change amounts to the widespread acceptance that the corresponding empirical results are replicable.(Collins [1992] p.129)
This means that working scientists never accept an interesting new claim on the basis of 'empirical results' which are not replicable.  If Collins is right, the favorable reception of Jackson's work by his contemporaries, and its influence on his successors are historical anomalies.
   I think the epistemological moral of Jackson's (and his contemporaries') use of poorly replicated data is that something is wrong with both the historical and the normative components of the received doctrine.  My view is that replication can be every bit as important as Popper and Collins thought in cases where it must be attempted in order to assess the reliability of the process by which a scientist produces and argues from a body of evidence.  But contrary to the received doctrine, I think doubts about reliability can often be settled by other means, and that sometimes, far from being necessary, replication is irrelevant to their resolution.  I think this is what Jackson’s deployment of poorly replicated evidence illustrates.  In particular, I think that:
	a]	Although Popper is quite right to emphasize the importance of intersubjective evaluations of evidence, Jackson and his contemporaries were often able to evaluate the evidence they argued from without replicating it.
	b]	Although some of Jackson's arguments depended for their cogency upon whether certain observed symptoms and lesions co-occurred by coincidence rather than because of systematic causal connections to a neural mechanism of interest to the investigator, replication was not always required (as 1, Popper's regularity condition) to rule out such coincidences. 
	c]	A 'scientifically significant effect' should be, or should be indicative of, something of considerable importance, e.g., something  against which a theory can be tested, or something a theory should attempt to predict or explain, or something which provides an explanation or a means to predict something which falls within the purview of  the relevant theory.  If this is what Popper means, then, contrary to (2) Jackson's research frequently involved scientifically significant effects which were not well replicated.
    	d]		Contrary to Collins, Jackson brought about significant conceptual changes--particularly with regard to questions about the localization of motor functions—through the use of poorly replicated evidence. 
	iii.	A Sketch of Jackson's theory about the organization of brain and its 
functions (JH)  and an epistemically sanitized sketch of some of Jackson's 
arguments for it.
   Jackson's Hierarchy (JH):  Ignoring details, JH looks like this: The CNS contains a large number of motor centers consisting of ganglia which act—singly or in combination—to initiate and control the movements of all of the muscle fibers and groups of muscle fibers involved in voluntary and non-voluntary bodily movements.  These include the contractions and extensions required for autonomic movements (including the beating of the heart and contractions and expansions of blood vessels), reflexes ranging in complexity from simple eye blinks and knee jerks to the elaborate combinations of reflex movements by which the eye tracks, focuses, and regulates the input of light as a moving subject watches a moving visual object, and finally, the movements involved in voluntary behavior. The motor centers are located in different  areas from the top of the brain down to the spinal cord.  They and their functions are organized hierarchically in a way which involves a great deal of redundancy.  The motor functions required for the most complex, highly coordinated, and voluntary behaviors are initiated in the motor centers located in convolutions of the cerebral cortex.  These motor centers constitute the third and highest level of the hierarchy.  Each of them sends fibers to, and receives fibers from, other motor centers on the same level.  They also send fibers to smaller motor centers in the convolutions of the cerebral cortex near the basal ganglia. These last comprise the upper part of the second (the middle) level of the hierarchy.  They send fibers down to the lower part of this level which includes the basal ganglia and the extreme capsule.  Jackson and his colleagues called these last the corpus striatum. (See n.9 below.)  Fibers from the corpus striatum descend to centers in the brain stem, each of which sends fibers down to still smaller centers in the spinal cord.  Every muscle fiber in every part of the body is innervated by one or more neural fibers which descend from the motor centers of the spinal cord.  These, together with brain stem motor centers belong to the first and lowest level of the hierarchy.  Fibers from first level motor centers carry what were variously referred to as "nervous discharges" "currents", "influences", "energy", "force" and "impulses" capable of causing the contraction or extension of the muscle fibers or fiber bundles to which they are transmitted.  As a result, any given muscle fiber will be connected directly to a motor center in the spinal cord and indirectly, by various relays to higher centers in the brain stem, the corpus striatum, and in many cases, the cerebral cortex and the cerebellum.  This means that neural activity in two or more anatomically discrete parts of the CNS above the level of the spinal cord may contract or extend one and the same muscle fiber or fiber bundle. Because every motor center above the spinal cord sends neural fibers down to a number of different lower level motor centers, different movements involving the same muscles can be produced by discharges from different motor centers in the brain stem and above.  If the nerve and muscle systems are in good working order, discharges from motor centers in and above the corpus striatum produce coordinated movements of the hands, arms, legs, etc. and of their parts.  Any single muscle fiber or bundle which participates in a complex body movement (the curling of one of the fingers involved in grasping an object, for example) by virtue of its connection to one upper level motor center may also participate in an entirely different and more complex motion (shaking hands, playing a trill on the piano, making a beckoning gesture) by virtue of its connection to another upper level center.  Although this paper will not be concerned with it, JH also maintains that the sensory systems are organized in an analogous way, and that motor and sensory centers at different levels of their hierarchies are connected both laterally and vertically , as required to allow for sensori-motor reflexes.
   Some arguments for JH:  For convenience of exposition I'll begin by sketching some of Jackson's arguments without mentioning their epistemically problematic details. The troubles, and their relevance to the received doctrine are taken up below (§iv, ff.).
   Jackson said he analyzed the symptoms and pathology of epilepsy not just to locate brain lesions which caused its symptoms, but more importantly, to 
…study the relations of epilepsy or epileptiform seizures to simpler diseases of the nervous system, and through the latter to normal states. Jackson[1958 I]p.165)
   Some terminological points are in order in connection with this and other passages from Jackson which I'll be discussing.   According to present day usage, epileptic seizures are hypersynchronous, self maintaining neuronal discharges which disrupt sensory, motor, and other psychological functions.   For Jackson, they are sudden, excessive, transitory discharges of some part of the cortex. (Jackson[1958 I], p.8; [1958 II], p.9). Both characterizations pick out abnormal brain activities which cause a variety of symptoms including epileptic auras (e.g., sensory hallucinations, feelings of dizziness, tingling or prickling sensations in arm or leg muscles), dreamy or absent states of consciousness, and convulsions.  The main difference between ours and Jackson's notion of the epileptic seizure is that we have a much better idea of what the abnormal activity consists of, and of how to detect and measure it. (We know a great deal more than Jackson knew about the relevant electrochemical mechanisms.  While we have electroencephalogram and related techniques for recording abnormal electrical activity in the brain, Jackson had to infer its occurrence and guess at its strength from convulsions and other symptoms).  Either characterization of the epileptic seizure will do for what follows in this paper.  
   According to present day (as well as common19th century) usage the term 'epileptiform' is used in connection with cases in which symptoms which are typical of epilepsy are produced by some other cause.  Jackson, by contrast, used the term in connection with seizures featuring convulsions which begin in one part of the body—usually a hand or a foot--and gradually spread up the limb and on to muscles in other parts of they body. The march of the spasms sometimes stops by itself, and may sometimes be stopped by pressing the affected limb above the convulsed muscles.  But where this does not happen, the subject eventually falls to the floor in a comatose state.(See §iv below for some case history descriptions).  It was due to Jackson that these seizures came to be thought of as  genuinely epileptic.  In honor of his work, they are often called 'Jacksonian seizures' and this is how I will refer to them in what follows.  (In passages from Jackson cited below, 'epileptiform' should be understood to mean Jacksonian). Jacksonian seizures contrast with "drop fits".  In what follows I'll use that informal term for seizures in which convulsions develop all over the body so quickly that they appear to begin simultaneously, and the patient loses consciousness almost immediately,  Because they develop gradually Jacksonian seizures  provide a better opportunity for the clinician to observe the details of distinct motor symptoms than drop fits.
   In the passage just cited Jackson said he was interested in connections between 'epileptiform' (i.e., Jacksonian) seizures and simpler diseases of the nervous system.  One of those simpler diseases is hemiplegia—weakness, partial paralysis, or full paralysis of the arm, leg, or face on one side of the body.  The following are some examples of what Jackson believed a study of relations between Jacksonian seizures and hemiplegia can teach us about the normal functioning of the CNS. 
   According to Robert B. Todd's textbook on neuro-physiology, a standard reference for several years after its completion in 1847, it is a well established fact '…of strong import in reference to the motor functions of…' the parts of the brain which go to make up the corpus striatum, that a '…lesion, even of slight amount..' in the corpus striatum invariably causes paralysis in some part  of the body. (Todd [1839-47] p.722)  What Todd said about this is wrong, but Jackson took only minor exception to it.  Along with most of his contemporaries he believed  that hemiplegia is due to the inability of tissue in the corpus striatum to discharge the nervous energy required for voluntary (as opposed to convulsive) movements of the affected limb.  
   As far as I have been able to tell, the best available evidence for this consisted of post-mortem findings of hemorrhages, clots, and other circulatory pathologies near the corpus striatum (and in at least one case, the abnormal appearance of tissue in the corpus striatum itself) of hemiplegic patients.  Jackson supposes that interruptions of the blood supply render tissue in the corpus striatum incapable of discharging the nervous force required for normal movement by depriving it of the nutrition required for proper function.(Jackson [1958 I], p.94, 96-7, [1958 II], p.54, p.239)  The inference from the post-mortem findings to the general claim that corpus striatum lesions cause hemiplegia depends in part on the assumption that
		Each movement disorder (convulsion, paralysis, chorea, etc.) of a specific part of the body has as its cause at least one physiological lesion in some 	specific, anatomically discrete region of the CNS.  
   Jackson uses the term ‘lesion’ in connection with two importantly different kinds of abnormality: [a] physiological or functional abnormalities—hyperactivity, depressed activity, or inability to discharge--of a particular bit of neural tissue and [b] pathological abnormalities—e.g., clots, embolisms, tumors, which can render neural tissue overactive, underactive, or inactive.(Jackson[1958 I], pp. 29ff)  'Physiological lesion', is my term for the former; 'pathological lesion' is my term for the latter.  Some  pathological lesions are located in exactly the same anatomical structures as the physiological lesions they cause.  For example, dead neural tissue cannot discharge or transmit neural force.(Jackson[1958 I]p.25, p.144)  But Jackson's post-mortem data often featured pathological lesions (e.g., in a blood vessel) which he interpreted as responsible for physiological lesions elsewhere in the brain.  Furthermore, physiological lesions of the same kind can be produced by a variety of different pathological lesions.(Jackson[1958 I]p.221) The lesions which correspond to specific motor symptoms, including the corpus striatum lesions Jackson thinks are responsible for hemiplegia, are physiological rather than pathological.  Thus Jackson's views on the corpus striatum can be accommodated to the fact that most of the relevant pathological lesions he argues from are located outside of the corpus striatum.
   Let us turn now to some of Jackson's arguments.
		A1: An argument from temporary post seizure paralysis in limbs which had convulsed during a Jacksonian seizure to the conclusion that paralysis and convulsion may be caused by lesions in the same part of the brain.
  According to Jackson, if the inability of corpus striatum tissue to discharge causes loss of motion or weakness in a given part of the body then if, instead of failing to discharge, the same bit of corpus striatum tissue had discharged excessively, that part of the body would have convulsed.  In general, he thinks,
… mobile conditions of the face, arm, and leg (an epileptiform seizure in which these parts are convulsed, or irregular movements of them as in hemichorea) are owing to nervous discharges in the very same cerebral region [whose failure to discharge would have produced weakness or paralysis]. (Jackson[1958 I]p.165; See also pp.67,163).
   One piece of evidence for this supposition, says Jackson, is that in some patients, Jacksonian seizures are followed by temporary hemiplegia which is found in the same part of the body in which the Jacksonian convulsions began (Case 5, iv, below, is an example.)  Jackson supposes the only condition which could cause post convulsion paralysis or weakness from which the patient recovers in a relatively short time would be fatigue resulting from the overactivity of nerve tissue whose excessive discharging caused the convulsions which preceded the hemiplegia.  As soon as the overworked neural tissue recovers from its exhaustion it can respond normally when the patient tries to move the affected limb.  This accounts for the temporary nature of the paralysis or weakness.(Jackson[1958 I]p.25,144ff.)   If the part of the brain whose fatigue caused temporary, post-convulsion hemiplegia were different from the part whose excessive discharge caused the convulsions, the motor disturbances should not have occurred in the same place.  The more distant the physiological lesions, the farther apart Jackson would expect the afflicted parts of the body to be.  Thus the fact that convulsions and paralysis or weakness are observed to occur in the same part of the body argues that they are caused by physiological lesions in the same part of the brain.  If the corpus striatum is always involved in hemiplegia, then the tissue whose excessive discharge causes Jacksonian convulsions should also be in the corpus striatum. 
   This would be unconvincing if alternative explanations for the paralysis were available. Jackson addressed two of them explicitly.  One alternative was that the paralysis resulted    
… from the cerebral congestion of asphyxia induced by arrested respiration in the paroxysm. (Jackson, [1958 I] p.319)
Jackson rejects this because congestion due to asphyxia should occur all over the brain and therefore 'cannot account for local paralysis.'(ibid.)  The second alternative he rejected was that the paralysis is due 
…to small extravasations of blood caused by congestion from arrested respiration.(ibid.)  
When a Jacksonian seizure is followed by temporary paralysis, the loss of motion always occurs in the limb where the convulsions began.  But 'it would be very remarkable' argues Jackson, if the small extravasations responsible for the paralysis according to the alternative account always occurred in just the right place to debilitate the limb which convulsed first.(ibid.)
   Absent further alternative explanations of the temporary paralysis, its occurrence in the limb where the convulsions began argues for Jackson's position.
   A2:  Discounting and reclassifying observations of drop fits which seem to be inconsistent with Jackson's account of convulsions in temporarily paralyzed limbs.    
   It is a difficulty for the argument just sketched that observers of drop fits do not report temporary post convulsion paralysis.  How could the nervous discharges responsible for Jacksonian convulsions produce enough motor center fatigue to cause hemiplegia if drop fit discharges fail to do so?  Jackson suggests two ways in which the absence of reports of hemiplegia after drop fits can be accommodated to his supposition that convulsions can fatigue motor centers sufficiently to cause weakness or paralysis.  First, he suggests that clinicians do observe temporary paralysis immediately after severe fits in which the patient loses consciousness only to misidentify what they see.
After a very severe fit of epilepsy proper, the patient does not move his limbs; all admit that.  He seems a mere breathing, circulatory, etc., mechanism, lying otherwise inert on the floor.  As he is thus comatose, it would generally be said that he does not move because he is unconscious.  A moment's reflection will show that this…explains nothing…I submit that the post-epileptic comatose patient does not move, for the very simple reason that there is some negative physical condition of his nervous centers.(Jackson[1958 I] p.322)   
The negative condition, he thinks is extreme, widespread motor nerve fatigue.  The resulting paralysis is not limited to one side of the body because the convulsions occur (and therefore produce fatigue) all over the body.  Perhaps because it is not localized, people  think the coma is due to loss of consciousness and fail to realize the paralysis is due to motor center fatigue.
  Secondly Jackson suggests that once the coma is over and the patient is able to get up and move around, there may still be paralysis or weakness which goes unobserved because it is widespread and relatively mild.  The patient does not suffer from '…any paralysis of but one limb; he is not hemiplegic'.(Jackson [1958 I] p.321)  But Jackson supposes that the nearly simultaneous, widespread, bilateral convulsions of a drop fit exhaust and therefore temporarily paralyze muscles all over both sides of the body.  The resulting paralysis goes unnoticed because it is '…slight, evenly spread, and transient'. (ibid.) This would be because, instead of forcing any one motor center to discharge long enough to exhaust it completely, the seizures of a drop fit pass rapidly through the body affecting all of its motor centers evenly for a very short period of time.  Once the coma is over, the results of exhaustion are too mild and evenly distributed to be 'easily recognizable as paralysis', and this would account for their not being observed..
	A3:	An argument for the claim that the normal motions of the legs, the arms, and the face are all represented in the corpus striatum.     
   Jackson says the study of hemiplegia, convulsions, etc. 
…is really the study of cases as departures from healthy states.  For hemiplegia may, for this purpose be properly regarded as an experiment made by disease revealing to us the external parts represented in the healthy corpus striatum.  It shows that the corpus striatum contains nervous processes for the movements of the face, arm, and leg.  The unilateral convulsion and the hemichorea are over-developments of such movements which are lost in the quasi-experiment of hemiplegia. (Jackson[1958 I]p.165) 
   When Jackson says that 'the corpus striatum contains nervous processes for the movements of the face arm and leg', or (as he usually puts it) that motions of a part of the body are represented or contained in a part of the CNS, he means that when the relevant nerves and muscles are in good working order,  movements of the face, arm, and leg  are caused by discharges in the corpus striatum.  By extension,  a part of the body (as opposed to its movements) is said to be represented in any region of the CNS which contains representations of its motions. (Jackson[1958 I] p.p.428)  Thus a part of the brain containing neural tissue whose normal discharge is sufficient to cause a given movement is said to represent, or to contain representations of that movement.  And a part of the body is said to be represented in any part of the brain which represents its movements. 
   Now, assume that 
		 The motions of any specific part of the body are represented in every motor center whose physiological lesion would render those motions abnormal (by causing convulsions, paralysis, or weakness, or by disrupting normal sequences of motions to produce chorea, ballismus, etc.).  (Jackson[1958 I]p.114, [1958 II] p.29ff)
   Then, if both hemiplegia and Jacksonian convulsions of the arms, legs and face are due to physiological lesions of the corpus striatum, we have reason to believe that movements of the face, arm, and leg are located in the corpus striatum.
   The next arguments I want to consider were directed against two views which are incompatible with JH.  Jackson calls proponents of the first view 'localizers'.  (Jackson[1958 II]pp.34-35) They maintain that no two motor centers represent the same part of the body.  Jackson holds, contrary to the localizers, that no motor center or
…. part of a motor center represents exclusively any limited region.  To illustrate, there is no cerebral center for the arm only, nor is there one for the leg only.’(Jackson[1958 II]pp.29-30) 
His view is that
		Multiple location: the movements of any given part of the body are represented in more than one motor center.(Jackson 1958 I]p.70)  In particular, movements of single muscle fibers and bundles of  muscle fibers which are represented in the spinal cord and the brain stem are re-represented in the motor centers in the corpus striatum, and again in the cerebral convolutions near the corpus striatum, and again in the highest motor centers at the top of the brain.(Jackson [1958 I] p., 26, [1958 II] pp.29—43)
For example, Jackson supposes that every 'term' or 'unit' (by which he means a sufficiently large sub part) of the corpus striatum is connected by its descending fibers, and by the lower centers they innervate, to muscle fibers throughout the arm, as well as the leg and face.  That is why neither the corpus striatum, nor the higher centers which innervate it are, or contain terms which are dedicated exclusively to the arm, or the leg. 
   The second view Jackson opposes is that of theorists he calls universalizers who say that the same part of the body may be represented in the same way by every subpart of a cortical motor center.(Jackson [1958 II]pp.33-34]  His view is  that
		Uniqueness of Representation:  No two terms a motor center represent the same region of the body in exactly the same way.  Recall that to represent part of the body is to represent its motions.  To represent a given limb in the same way would be to represent exactly the same motions for that limb.  According to uniqueness of representation, the normal functioning of any two terms which represent, e.g., the arm, the hand, or a finger, will cause different motions in the relevant body part.  Thus one term of the corpus striatum will connect to nerve fibers from a great many muscles of the fingers, less in the upper arm, and still less in the face, while another will connect to many more muscle fibers in the upper arm, and relatively few in the fingers or the face.  And so on for the rest of the region.(Jackson[1958 II] pp.35,216 )
    Jackson assumes that the spatial and temporal ordering of normal motions are determined by, and are therefore indicative of the architecture of the motor system.
Coordination in Space—the power of using several muscles together for one purpose—is brought about by groupings of [neural] fibers.  Coordination in Time—the process by which one movement follows another [in such complex movements as grasping, lifting, and moving an object]—is brought about by relations of ganglion cells.(Jackson[1958 I], p.27; See also p. 36, and (Jackson[1958 II], p.248)
If in causing motion disorders, physiological lesions affect the functions of motor centers without altering their architecture, Jackson's data on the spatial and temporal orderings of convulsions, of the motions lost in temporary or permanent hemiplegia, and of motions acquired in recovery from hemiplegia can provide evidence for the anatomical and physiological relations between the motor centers in the normal nervous system. (See (Jackson[1958 I], pp. 69, 263; [1958 II], p.248).
   A4:  Evidence from the the order in which Jacksonian convulsions spread.   
Recall that in contrast to drop fits whose convulsions occur nearly simultaneously all over the body, Jacksonian convulsions typically begin with  tremors in an extremity and spread continuously  up the limb, sparing no part of the body along the path of its march.  The convulsions may spread from a finger to the arm, the leg, to parts of the face on same side of the body, and to the chest.  The convulsions may eventually spread all over the body until the victim loses consciousness.  The hand or foot where the fit begins continues to convulse, and its convulsions go stronger, as spasms spread along the limb and on to other parts of the body.  Each affected part of the body continues to convulse as the convulsions spread to new parts. .(Jackson[1958 I] p.6—11, 263-273)  This is congenial to Jackson's views.  Indeed, it is exactly what should happen if every term in the corpus striatum, or of the cortical motor centers which discharge into the corpus striatum represents different motions of muscles throughout the hand, arm, leg, etc. and the seizure begins, e.g., with abnormal activity in a term which represents a great many muscle fibers in the thumb, fewer in the rest of the hand, still fewer in the forearm and so on.  If this is were the case, the abnormally functioning term could discharge enough nervous energy to convulse the thumb without discharging enough to convulse the rest of the hand, the arm, etc.  This would explain why the thumb convulses before the rest of the hand; the more thumb motions a corpus striatum unit represents, the less nervous energy that unit should have to discharge to convulse the thumb.  As the seizure became more severe, more nervous energy would be discharged into the affected part of the corpus striatum—enough to move the other, less well represented parts of the body, to maintain or intensify  the convulsions of the thumb, and to cause seizure activity elsewhere in the corpus striatum or the cortical tissue which discharges into it. This is multiple location and uniqueness of representation could account for the way Jacksonian seizures spread. (Jackson [1958 I], pp.27-8, 69, 91, 333)  
   But although the evidence is suggestive, Jackson observes that it could also be accounted for by the localizer.  It could be that each muscle is uniquely represented by its own small motor center and that during a Jacksonian seizure, these centers begin their discharges one after the other (each one continuing to discharge as the others begin to release nervous energy) in a sequence which accounts for the march of the convulsions.(Jackson [1958 II] p.34)
	   A5:  An argument for multiple location from its ability to account for some paradoxical clinical and experimental evidence.   
    If the movements of each body part are multiply located, this would solve an outstanding clinical puzzle which the localizer cannot solve.  Some patients with long term hemiplegia experience convulsions in the very limbs which are paralyzed.  In cases where the paralysis is long lasting, and does not begin right after convulsions, it is plausible that it is caused not by fatigue, but by a permanent loss of  function in corpus striatum motor centers whose proper functioning is required for normal, voluntary motions. The  convulsions are puzzling because neural tissue which cannot discharge cannot cause muscle contractions.  If the localizers are right and the limb is represented by no more than one motor center, none of the motor centers which retain their ability to function could produce its convulsions, and the puzzle is insoluble.  
   But it can be solved if every motion of the affected limb is represented in more than one motor center.  Suppose the motions of fibers in each muscle are represented in different parts of the corpus striatum, in two or more motor centers higher up in the cerebral cortex, and also in the motor centers further down in the brain stem and spinal cord.  Suppose also that in order for someone to move a limb voluntarily, a cortical motor center representing the desired motion must discharge into the agent's corpus striatum, and in response, corpus striatum tissue must discharge into lower motor centers whose nerves innervate individual the muscle fibers in the limb to be moved.  Because paralysis is the inability to move voluntarily, a lesion can paralyze a limb by rendering some parts of the corpus striatum unable to respond to normal discharges from the cortex.  Next, Jackson supposes that a corpus striatum lesion can be sufficient to paralyze a limb without debilitating the rest of the corpus striatum.  Then motor nerves which innervate different muscles in the paralyzed limb could be activated by neural discharges in the parts of the corpus striatum which can still  function.  During a seizure, the activity of a number of higher motor centers produces disorganized and abnormally strong discharges in unharmed portions of the corpus striatum which represent fibers in different muscles the paralyzed limb.  The convulsions of paralyzed limbs consist of the resulting uncoordinated muscle contractions and flexions. (Jackson[1958 II] p.33)  
   It counted in favor of this account that cortical pathological lesions near the corpus striatum were found in a few autopsies of  patients whose permanently paralyzed limbs had been subject to convulsions.  The plausibility of this account and its ability to explain what the localizers cannot explain counts in favor of Jackson's view that the motions of a given limb are represented in more than one motor center.(Jackson [1958 I] pp.25ff., 30ff., 33, 244, 399ff.)  
   Jackson treated a related clinical puzzle along the roughly the same lines.  The puzzle is that 
 …destruction of parts of the convolutions in the neighborhood of the corpus striatum may produce no obvious paralysis, whilst the epileptic discharge of those parts would produce severe convulsion.(Jackson
[1958 I]p.144)
If the excessive discharge of a square inch of grey matter in the cerebral convolutions near the corpus striatum causes convulsions in the leg, that square inch must represent the motions of a great many muscle fibers in the leg by way of its connections to neural fibers in lower level motor centers.  The failure of the destruction of that same square inch to produce noticeable paralysis or weakness argues that muscle fibers in the leg are also represented in other motor centers in the convolutions.(Jackson[1958 I]pp.27ff, 66ff, 212, 214-217, [1958 II]pp.31ff, 35ff, 41ff, 55, 83, 216ff.)  Multiple location also promises a similar solution to an outstanding experimental puzzle—the fact (established by Fritsch, Hitzig, and Ferrier) that in dogs and other animals, no weakness or paralysis was observed after the destruction of a bit of cerebral tissue whose stimulation activated specific muscles in one of the animal's limbs.
   A related piece of evidence for Jackson's treatment of the puzzles comes from autopsies in which the investigator is able to identify parcels of neural tissue which cannot discharge (e.g., by inference from observable abnormalities in the motor tissue, or from its location relative to a pathological lesion which could disable it). Lesions of a certain size were found in the brain stems of some hemiplegics.  But lesions as large or larger were found above the corpus striatum in the cortical hemispheres of some patients who had not exhibited any observable paralysis or weakness.  This is what we should expect according to Jackson's theory.  Suppose a substantial number of muscle fibers belonging to some muscle are innervated entirely or mostly by nerves descending from a relatively small, lower level motor center, m.  Then, according to JH, that muscle will be paralyzed or weakened by a lesion in m.  But according to multiple location, no group of muscle fibers is innervated exclusively by nerves connected (by way of a lower motor center) to any single parcel of higher level motor tissue of roughly the same size as m.  Instead, a number of anatomically distinct, higher level motor centers send nerves down to m (along with other lower level motor centers).  A lesion in just one of these higher centers will not prevent the others from discharging into m as needed for voluntary movement.(Jackson [1958 I] pp. 26-27) 
   A6:  An argument for multiple location from observations of partial recoveries from long term paralysis.    
   Jackson has reports of some patients who recover some of their strength or some of their ability to move a limb which has been weakened or paralyzed for so long that its symptoms cannot be explained by fatigue.  Accordingly, Jackson supposes their loss of motion is caused by irreversible physiological lesions.  If so, he thinks, the recovery must be accounted for by the patient's having learned to use undamaged motor centers he had not previously relied upon.  Suppose the lesion is in a lower motor center which controls some of the muscle fibers the patient used to use to grasp things with his hand.   The patient could regain or strengthen his grip by acquiring through exercise and practice the ability to use other muscle fibers whose activity is represented by healthy neural tissue.(Jackson [1958 II]pp.35ff.)  He will not be able to grasp objects in exactly the same way, or with exactly as much strength as previously because he will not regain the use of the same muscle fibers.  That is why such recoveries are partial rather than complete.  Absent alternative explanations, the recovery evidence argues that the motions of any given part of the body are represented in more than one motor center.
   A7:  An argument from evidence concerning the locations at which Jacksonian convulsions typically begin for the claim that every term in a motor center represents motions throughout the part of the body represented by the motor center it belongs to.
Fits beginning in the hand are common, fits beginning in the cheek and tongue are less frequent, fits beginning in the foot are rare….again, taking numbers of cases, the fits which begin in the hand begin usually in the index finger and thumb; fits which begin in the foot begin usually in the great toe.(Jackson[1958 I], p.10) 
Jackson takes this as a reason to think that thumb and forefinger motions are represented throughout the corpus striatum (Jackson[1958 II], p.216)  He doesn't say why, but here is what he may have had in mind.  Suppose every bit of the corpus striatum has as good a chance of suffering a physiological lesion as every other bit of the same size. If so, (barring coincidences or elaborate hidden connections between the rest of the corpus striatum and a motor center for the thumb or forefinger) there is no reason why so many Jacksonian convulsions begin in the thumb and forefinger  unless they are represented more widely throughout the corpus striatum than motions of the face and tongue, and still more widely than motions of the foot.  If this is so, it is plausible that at least some of the terms of the corpus striatum which represent the face or the foot represent the hand as well. 
	A8:	An argument for multiple location and uniqueness of representation from the effects of the destruction of any sufficiently large part of the corpus striatum.  
[w]hen a sufficient quantity of any part of the corpus striatum is destroyed, the arm is permanently weakened or completely paralyzed. But it must not be overlooked that the limb is "partially paralyzed".(Jackson[1958 II], p.244]
By 'completely' paralyzed, Jackson means that no part of the arm is spared.  Jackson infers from this 
…that the muscular system of the arm—the whole of the arm movements—is represented in each part of the corpus striatum.(ibid.)
   By 'partially paralyzed' Jackson means that although every part of the arm is paralyzed to some degree, some parts have lost more motion than others.  This supports the claim that no two motor centers represent the same part of the body in the same way.
   A9:  Another argument for the claim that no two motor centers represent the same part of the body in the same way from observations of the development of motor abilities in patients who recover from long term paralysis.
   We saw (A6) that a hemiplegic patient may regain the ability to move parts of the body whose paralysis was due not to fatigue, but, rather, to permanent loss of function in one or more motor centers. (Jackson[1958 I], n.1, p.44)  But the recovery is never complete; the motor abilities the patient achieves are not exactly the same as the ones that were lost.(Jackson[1958 I], p.173, [1958 II], p.36)  Except where loss of function is due to fatigue, no motor center can regain its ability to discharge or to transmit a neural current once it has lost it.  Thus the muscles whose motions are restored must be represented in at least one motor center which retains its function in addition to the centers whose loss of function caused the paralysis.  If the motions represented by the diseased and the healthy motor centers were exactly the same, the recovery would be complete.  The fact that recovery is not complete argues that different centers which represent the same muscles do not represent them in the same way. (Jackson[1958 II], pp.36, 75)
	A10.	An argument for multiple location from fits in which the same muscles convulse but the convulsions develop in opposite directions.
   Jackson reports observations of
...two varieties of fits, in each of which, so far as I [Jackson] can learn, the same muscles are involved.  But in each they are involved in a different order.  The range is the same; the sequence is different.  Thus one man's fits begin in his hand, go up his arm and down his leg; another man's begin in his foot, go up his leg and down his arm. (Jackson[1958 I]p.70; cp. p.23)
 If the anatomical architecture of motor centers determines the sequence of muscular motions produced by their discharges, the fact that although
…the same motions are in action in each of the two fits, …[different] parts of both limbs are involved in a different order, and probably to different degrees renders the inference irresistible that the two fits depend on discharge of two different centers.(ibid.) 
 The difference between the two fits argues that the motor center responsible for one fit represents the convulsed muscles by representing a different sequence of motions than the motor center which is responsible for the other fit.
	iv.	Some examples of Jackson's evidence 
   As sketched above Jackson’s arguments seem to be ingenious deployments of carefully observed, solid empirical evidence. And so they seemed to many of his contemporaries.  Not everyone agreed with the conclusions Jackson drew from his data, but I haven't found anyone who questioned the data itself.  There's no doubt that Jackson's deployment of his evidence is ingenious.  But according to the received doctrine a lot of his evidence is too poorly replicated to be scientifically acceptable.
  Jackson’s clinical data consisted for the most part of descriptions of the symptoms of patients he treated at the National Hospital. Some of it reports his own observations. Here, for example is his description of a seizure suffered by a 48 year old male Jackson saw when, by happy accident, he happened into a room where the patient was waiting for an examination just as the convulsions began.  Jackson’s description features one of the instances of recovery from temporary post-convulsion paralysis which he used to argue (A1) that if corpus striatum tissue whose discharges cause convulsions in a given part of the body were to lose its inability to discharge, the same part of the body would become weakened or paralyzed. 
Case 5.--Partial convulsions beginning in the right hand.
   This case has to me a very great interest because I witnessed the paroxysm.  The march of the spasm was very deliberate: the time  occupied was about ten minutes.  Seven of these minutes were measured by the watch, the rest were guessed...his right hand began to twitch, the thumb and index finger taking the lead.  The fingers were soon partially flexed in a curve, except the index, which was straight, but flexed at its metacarpal joint; the thumb was straight too, but flexed also at its metacarpal joint, and lay with the palmar surface of its terminal segment against the side of the index finger.  Next the whole arm twitched, but it did not rise; the exact sequence of involvement of its several parts was not ascertained as the man was dressed.  In about two minutes...the right side of his face began to twitch, but before movement of it was discernible the patient said he felt "it" in his face.  The right eye was closed, the right cheek was drawn up, and both jaws came together.  The mouth was drawn up to the right (but whether before or after the meeting of the jaws was not noted), and its opening was ovoid, the wider end of the ovoid being to the right.  The right ocular aperture was a little closer than the other, but both were narrowed.  Both sides of the forehead were wrinkled upwards.  There was no deviation of the head nor of the eyes; the leg was not affected, and the patient could talk in any part of the fit.  He begged me to let the porter take hold of his hand--to unclench it--as the porter could manage it better.  The fit ceased very suddenly.  After the attack the arm, which was weak before the fit, was completely paralyzed, quite limp, and fell forward when he stooped, and it had not recovered completely when he left the hospital fourteen days later.  The patient's speech was not distinct before the fit, but was worse after.  It is not possible to say anything more definite about his speech than this, as the patient was a foreigner; what he said could not be made out.(Jackson [58] vol. I p.17-18)
   As the first line of this passage suggests, Jackson could seldom be at the right place at the right time to observe a fit whose symptoms would be of interest.  He often had to rely on the reports from others, including  the patients themselves. Here is Jackson's summary of a patient's report.
Case 4.--Seizures, partial and severe, beginning in the right thumb.  Arrest by ligature....
   A single woman, 22 years of age, consulted me…for fits.
   Each fit begins by movement in the thumb of the right hand, and by degrees the whole arm is involved.  The same side of the face is drawn, and the head is drawn towards the arm, which is raised to meet it.  The patient's remark is, "it seems as if it wanted to draw the arm into the head."  "It" goes to the leg after the face has begun to work, and then she becomes insensible; the insensibility she ascribes to the severe pain in the muscles ("sinews" is the word she uses).  This observation is of value as showing that the pain from the cramped muscles is severe.  She foams at the mouth and bites her tongue.  When she comes to herself she speaks well.  She cannot walk well after the attack, but this is attributed to giddiness and headache.  She says the right arm is affected, but only slightly  There is at least no decided hemiplegia after the seizures…She has slighter seizures, or, as she said at the next visit, "I have had no fits, but the hand has been very fidgety, and I have had to tie it up twice."…She added, "But it (the tying) makes me feel giddy." ...on January 4, 1870, she had a fit of intermediate severity.  To use her own words, she had "workings of a fit" but did not become insensible.  The spasm affected the arm and the side of the face a little.  It did not get to the leg, and there was no drawing of the head to the right.  The arm was "tied up"; first a ribbon was tied around the middle of the forearm, and, as this "would not stop it" the ribbon was next tied around the middle of the upper arm--"this kept it from taking my senses away."  The arm was "tied up" for two hours; for when untied "it drew up"; when tied it kept quiet.(Jackson [58 I] p.15)
   These excerpts are representative of the clinical data Jackson worked from.  Observations were replicated only in the sense that Jackson and others sometimes witnessed variations on roughly the same  general themes. They observed or obtained descriptions of Jacksonian fits which began in the extremities, but not always the same extremity.  The convulsions moved up the body, but they did not all progress at the same speed or to the same point.  Some, but not all, were preceded  by auras and accompanied by additional symptoms, but not of the same kinds. There were in addition differences in age, general health, state of nutrition, medical history, and other factors which would seem to be relevant to the workings of the disease. Some of the details which Jackson's arguments emphasized were observed infrequently; a few were observed only once or twice.  Neither Jackson nor his colleagues had many opportunities to observe complete fits from beginning to end.  A patient's clothing often obscured the observer's view of convulsive movements.  A patient's accent might obscure speech abnormalities.  In Short, Jackson's clinical evidence is scanty, and at best poorly replicated.  
   The post-mortem evidence seems no better in these respects.  A number of patients whose symptoms had been especially interesting or well observed were discharged from the hospital  and never autopsied.  Some who died in the hospital were not autopsied because consent could not be obtained.  The resulting gaps in the pathological record produced epistemic frustrations reminiscent of difficulties raised for evolutionary theorists by gaps in the fossil record. To make matters worse, similar brain lesions reported in autopsy records were often accompanied by a variety of additional pathological abnormalities.  And some lesions which (judging by the autopsy reports) were very similar, belonged to patients who exhibited noticeably different groups of symptoms.  
   Jackson supervised some of the autopsies, observed others, and participated in a few.  But he did not see all of the autopsies he appeals to, and he did not write many autopsy reports himself.  Although it was very important to Jackson's research program to find correlations between kinds of symptoms and kinds of pathological lesions, case histories and autopsy reports were often written by different people.  Different writers tended to emphasize different things and to describe them to different degrees of detail.  Autopsies were almost never performed immediately after death; some had to wait long enough for tissue deterioration to obscure significant pathological signs and to raise doubts about whether all observed abnormalities were present before death.  In general the post-mortem evidence comes no closer to satisfying Popper's repeatability condition than the clinical evidence.  
   And it is hard to think of plausible but less stringent conditions under which they would qualify as well replicated.  Of course it might be that such evidence was replicable in the sense that had things been very different (if all the fits could have been witnessed from start to finish, if all of the interesting cases could have been properly autopsied immediately, etc.) interesting observations would have been repeated.  But this sort of counterfactual replicabiltity is epistemically irrelevant.  Replicability can't be used as a standard to evaluate evidence unless there is some way to tell whether the evidence is replicable.  But under the circumstances in which Jackson worked, the relevant counterfactuals could not be evaluated, and could therefore play no role in the assessment of Jackson's arguments.   
	v.	Replicating experiments; replicating data; replicating "effects"
   In order to see how the received doctrine applies to Jackson's methodology we need to attend to a distinction--ignored by Popper, Collins, and others-- between some importantly different sorts of replication:  
	a]	 Procedural Replication:  The same experimental or observational procedure may be repeated in order to obtain data required for such purposes as calibrating a measuring device, identifying  systematic sources of error, estimating ranges of randomly produced error, or for statistical evaluations of claims about causal mechanisms.  Repeated applications of the same experimental or observation procedure typically do not, and are not expected to, produce exactly the same results.  Although replications of the relevant procedure are required, a result obviously does not need to be thrown out because it differs from previous results.  Lacking instruments to calibrate, and investigating, as he was, grossly qualitative phenomena whose detection and identification do not require the statistical analysis of sets of quantitative data points, Jackson had no need to repeat the application of observational or experimental procedures for purposes like the ones just mentioned. 
   In this respect, it is worth contrasting Jackson's work to that of present day neuro-cognitive psychologists like Caramazza, Farah, and Shallice.  Ignoring details, these investigators are trying to produce fine grained accounts of the simplest and most basic cognitive functions, and their roles in the performances of complex everyday cognitive tasks.  To this end, they examine the performances of brain damaged subjects on a variety of numerically scored tests designed to isolate and identify specific deficits in discrete, relatively simple cognitive functions.  This is a highly sophisticated instance of the study of what Jackson and Bernard called 'the experiments made by disease'.  A number of serious obstacles must be overcome before anything can be learned from it.  First there is no guarantee that abnormally low scores on any given test will be due to a deficit in just one, rather than a number of distinct functions.  Secondly, a subject who is distracted, upset, bored, or uncooperative may perform badly on a test for reasons which are not indicative of a cognitive deficit caused by the brain lesion.  Thirdly, what appear to be interesting correlations between scores on several different tests may be due to coincidence, to theoretically uninteresting common causes, or to artifacts of the testing procedures.  Because of such difficulties, each patient must be given the same tests over and over until there is enough data to enable the investigator to determine through statistical analysis whether the scores are indicative of any significant features of the cognitive architecture.(See, e.g., Caramazza [1986], Shallice [1998], pp.21-41, Farah[1995] p.xv)  
   Jackson was not trying to investigate functions--let alone cognitive functions-- whose detection required the kind of fine grained analysis of observable behaviors which Caramazza and the others had to undertake.  The behavior deficits which interested him presented none of the observational difficulties which motivated the likes of Caramazza to repeat applications of  the same tests.  To produce the observational data used in the arguments I sketched in §iii, an observer needed only to notice motor abnormalities that are easy to identify (for observers who are lucky enough to get a chance to witness them), and tumors, blood clots, and other macroscopic brain abnormalities that are readily identified in the course of an autopsy.  There certainly were difficulties in the production of such data, but not the kinds of difficulties which required Caramazza, Farah, and Shallice to repeat the same experimental and observational procedures.  The problem was not e.g., that it was hard for a careful observer to tell whether an epileptic's arm convulsed after his hand.  One observation of a complete fit would suffice for that. The problem was that Jackson and his colleagues seldom had the opportunity to observe all the details they needed to observe.
   Procedural repetitions are to be distinguished from replications of the outcomes of applications of the same experimental or observational procedure.  Repeated applications of the same experimental or observational procedure typically do not produce exactly the same results. The epistemological questions Jackson's work raises for the received doctrine have to do mainly with replications of observations or effects rather than repeated uses of instruments or data production techniques.  
   We need to distinguish between two kinds of experimental and observational results which scientists may try to replicate.  As the language of Popper’s regularity requirement (1) suggests, experiments or observational procedures may be repeated in hopes of producing instances of the same (or impressively similar) observational data.  This is  
	b]	Replication of data.  It is to be distinguished from			c]	Replication of effects.  Judging from the language of his repeatability requirement (2) this may be what Popper had in mind.  
   The term 'effect' is usually used in connection with results produced by experimental manipulations.  I will use it for these, but also for results of natural occurrences and for some accidental or otherwise unplanned laboratory events.  As I am using the term, things as unplanned and uncontrived as solar flares, the extinction of the dinosaurs, the 1970 Rialto fire works explosion, and the unexpected glow Roentgen noticed on a screen at some distance from his carefully shielded cathode ray equipment qualify as effects, along with the expected results of well understood and carefully designed experiments.  Some effects, like the marches of Jacksonian convulsions from the extremities up the limbs, are observable in the sense that their detection requires little more than paying careful attention to what can be seen by observers who are at the right place and the right time.  But many scientifically important effects do not themselves register on human perceptual systems or the equipment scientists use to produce data for use in detecting them.  Unobservable effects can be detected by producing and reasoning from data.  By data I mean records of things which do register on the human perceptual systems or on observational and experimental equipment with which to detect them.  The detection of unobservable fluxes in the emission of solar neutrinos from Geiger counter data is an example of such detection.(Bogen & Woodward [1988],p.320ff.; Pinch [1985] pp.173--185) When Jackson reasoned from descriptions of blood clots observed during autopsies to conclusions about physiological lesions he was trying to detect an effect he could not observe--a bit of brain tissue's inability to discharge--from pathological lesion data. 
   Finally, repetition consisting of repeated instances of one and the same effect should be distinguished from 
	c']	Repeated detections of the same effect.  When  Lavoisier and Priestley killed mice by enclosing them in bell jars filled with fixed air (CO2) they were repeating an effect (suffocation) by repeatedly performing the same experiment and getting the same results.  But Lavoisier also discriminated oxygen from atmospheric air by reasoning from several different kinds of data which he obtained by performing experiments of notably different kinds.  For example, in addition to observing how long a mouse could survive in the gas he was studying, Lavoisier subjected it to Priestley’s “nitrous air” (nitric oxide) test for goodness of air, and also performed experiments to see how long candles would burn in it.  In doing this he was using different means to detect the same effect having to do with the chemistry of the gasses he was investigating.
   I think that the replication of data is often less important to real world scientific practice than the replication of an effect or its detection.  
   Jackson scores low marks for all of these kinds of replication.  According to Popper this should mean that Jackson’s work was epistemically flawed.  According to Collins, other scientists should not have accepted Jackson's theory.  But  the history of science is filled with examples in which scientists rely on evidence lacking in such epistemic values as truth, accuracy, and even logical compatibility with the theory they are used to support. That makes it natural to ask whether Jackson’s arguments are as bad as they should be according to the received doctrine about replicability.
	vi.	Jackson was not alone; some methodological lessons from Harvey and Bernard.   
  Contrary to the received doctrine, it is relatively easy to find cases of unreplicated or poorly replicated but epistemically valuable evidence.  In high energy physics, some important evidence for the existence of a weak force consisted of data which could not be regularly repeated—a small number of photographs of effects in bubble chambers, and a few spark  records indicative of weak neutral interactions among neutrinos and nucleons.  These effects seldom occurred at the right time or the right place or under the right circumstances for the photographic or other equipment to capture the signs from which they were detected.(Galison [1987], Chp.4)  As is well known, the data from which Millikan calculated the charge on the electron was notoriously irregular and hard to replicate. Although he finds it both surprising and in need of explanation, David Hull takes it to be a clearly established fact that even when data or effects are replicated, just a few repetitions may suffice to secure widespread acceptance for a theoretical claim.  For example,
The universality of Kepler's laws was accepted on the basis of a handful of observations of a single planet…Physicists did proceed to investigate the paths of planets other than Mars.  They were not especially surprised to discover what they expected…In testing, a point of diminishing returns is soon reached.  Additional observations that bear directly on the particular phenomenon at issue are not worth the effort.(Hull[1990] p.495-496) 
   These examples come from physics and astronomy, the very sciences Popper seems mainly to have had in mind when he wrote about replication.  The biological sciences provide further examples.  Thus one of the best pieces of evidence for adaptation is a single effect which has not been, and almost undoubtedly never will be, repeated.  Before the Industrial Revolution, the predominant color of a moth (Biston betularia) observed in Manchester was a speckled grey.  When its resting place became covered with soot, the predominant color changed to black. The black strain is supposed to have prevailed because it was harder than the lighter strain for its predators to spot.  (Mitchell [1987], p.354) The production of this effect required a particular sort of moth to be caught up in such a peculiar, large scale environmental change that to require replication here would amount to dismissing it out of hand.  
   Examples of influential, but poorly replicated evidence abound in the neuro-sciences.  I took the title of this paper from one of them.  After describing two post-mortem findings in support of a position he was arguing, WH Walshe, a contemporary of Jackson's, said he would offer no further instances because 
…these two suffice to make the point at stake as absolutely as a hundred might.'(Walshe[1849],p.279)
   William Harvey's use of a single, unrepeated observation to argue for the Aristotelian thesis that all arteries pulsate together because their pulsation depends on the heart is an especially instructive example of Hull's idea that multiplying observations that bear directly on a particular phenomenon need not be worth the effort.  I want to mention some of its details because it exemplifies a strategy Jackson was to use many years later, and teaches us something about why certain sorts of evidence and certain kinds of effects need not be replicated.
   Harvey noticed that the tumor (this was his term for the pulsating swelling) he found on the neck of one of his patients '…was distended with each rush of blood from the [subclavian] artery' and that even though the pulse in the patient's right arm kept pace with that of the tumor (the bulge) it was considerably weaker.  A post-mortem examination established that the tumor was an aneurysm (a ballooning caused by the blood exerting pressure on a weakened bit of blood vessel wall).  This, together with Harvey's background knowledge  of the anatomical relations between the relevant parts of the circulatory system convinced him that 
[t]he pulse in this same arm was small because the greater part of the blood to it was intercepted by the tumor.
According to Harvey this is an instance of the fact that 
		…[w]herever the motion of the blood in the arteries is impeded, by compression, by infarction, or by interception, there is less pulsation distally, since the beat of the arteries is nothing else than the impulse of blood in these vessels. (Harvey[1978]p.36-7)
Because this is just what should happen according to the Aristotelian thesis that all arteries pulsate together because their pulsation depends on the heart,  
it gave Harvey a reason to think that Aristotle was right. 
   Harvey reached his conclusion by inferring to a cause for what he observed.  He inferred that the influx of blood pumped into the arteries accounts for the pulse, and that the diversion of blood flow into the distended bit of the subclavian artery accounts for the weakness of the pulse in the arm beyond the swelling.  If his description of the patient is true with respect to the details described in the passages just cited, if an interruption of arterial blood flow can weaken the pulse further down the artery, and if nothing else was going on in Harvey's patient to account for the difference in the pulses, Harvey’s causal story is at the very least highly plausible.    
   In order to draw a general  conclusion from his finding Harvey had to suppose that the circulatory systems of normal humans are anatomically similar to that of his patient with respect to the features the causal story depends upon.  Here Harvey was on solid ground.  Even during Harvey's time enough evidence from post-mortem examinations of human beings was available to provide overwhelmingly good inductive support for the required assumption of circulatory system uniformity.  Indeed, there was enough evidence from dissections of other animals  to warrant Harvey in generalizing his conclusion to other species.  
   For my purposes, it is  important to distinguish [a] Harvey's reasons for believing that he had correctly observed and described his patient's pulses and that he had found the cause for the difference between them, from [b] his reasons for thinking he could base a general claim on this single case.  With regard to b, notice that the evidence for the relevant anatomical similarities between the circulatory systems of humans and other animals does not consist of repetitions of Harvey's observation.  Instead of reports of observations of the pulses of subjects with subclavian aneurysms, it consists of reports of observations of hearts and blood vessels of dead animals.  Secondly, notice that the question the post-mortem evidence is used to answer is very different from the question to which a repetition of Harvey's observation might be relevant.  The anatomical evidence is used to answer the question whether the Aristotelian thesis that all arteries pulsate together because their pulsation depends on the heart which seems to hold for Harvey's patient also holds for normal humans (and other animals ) as well.  It is obvious that repetitions of Harvey's observations would not support the generalization of the Aristotelian thesis.   Instead they would answer the question (had anyone asked it!) whether the pulse in the patient's arm really was weaker than the pulse in the swelling in his neck, i.e., whether what Harvey had reported was a genuine effect.  Thus we have on the one hand, considerations which are straightforwardly relevant to the question whether a putative effect is genuine, and on the other hand, considerations relevant to the question whether the observations used in an inductive argument have been drawn from a large enough, or a representative enough, sample to warrant a general conclusion about individuals who do not belong to the sample.  Replication is one way to test the correctness of an observational report or the genuineness of what someone claims to be an effect.  But I submit that it is not the only way, and that it is sometimes perfectly reasonable to accept the correctness of a report or the genuineness of a putative effect without it.  Examples of this from Jackson's and his colleagues' research will be discussed presently.  Repetitions of the same observation may also serve as evidence for an inductive argument.  But they are certainly not always necessary, and most epistemologists of science agree that in arguing for a theoretical claim, varied evidence is usually preferable to repetitions of the same evidence.  I think that repetitions of observations are typically of interest (when they are of interest) with regard to questions about the correctness of a report or the genuineness of a single effect.  I believe that the received doctrine about replicability owes some of its apparent plausibility to a confusion of these and very different questions about the adequacy of inductive arguments.   
   To return to Harvey's argument, a friend of the received doctrine might object that every patient with a similar aneurysm ought to exhibit a similar pulse pattern and therefore, that Harvey could have replicated his observations even though he didn't actually do so.  Furthermore, the objection would run, if Harvey had  tried and failed to replicate his observation, this would have discredited the inferences he based on his first observations.  This counterfactual replication requirement offers no comfort to Collins because he believed that actual  replications of evidence and effects are required to impress working scientists.   
   Does it help Popper? I think not.  Suppose we read Popper's repeatability requirement (2, p.4 above) as a disjunctive requirement according to which an observation, a bit of data, an effect, or the identification of an effect has no epistemic standing unless either it actually is ' regularly reproduced' when investigators 'carry out the appropriate experiment in the way prescribed' or it is the case that if investigators had carried out 'the appropriate experiment in the way prescribed' then the effect would have been 'regularly' reproduced—and similarly for data, and identifications of an effect.  There are cases (the case of the Manchester moths, for example) in which the counterfactual requirement provides no genuine epistemic test because there isn't any way to decide what would have happened if the relevant experiment had been attempted without appealing to the very claims the data or the evidence is used to support.  In Harvey's case, by contrast, the counterfactual can be evaluated, but there would be no epistemic point in doing so.  By the time Harvey did his work, enough anatomical and physiological uniformity among human and animal circulatory systems had been established to make it plausible that any competent observer of a patient with a subclavian aneurysm should be able to find the pulse pattern Harvey reported.  But what we really want to know is whether Harvey's evidence supports the general claim about how compression of an artery affects the distal pulse which Harvey used this to argue pulsation depends on the heart.  To find out about this, we ignore the counterfactual and apply instead the relevant background knowledge to evaluate Harvey's inference.  What was known about human anatomy and physiology, together with what was known about Harvey's abilities to observe and describe aneurysms, pulses, etc. makes it perfectly reasonable to accept Harvey's description of his observations.  The known uniformities argue that the circulatory system of Harvey's patient resembled that of other humans and animals in ways which support the general claim about the influence of arterial compression on distal pulse.  If there was some reason to do so, we could use the very same background knowledge in support of the counterfactual claim about what other observers would see if they took the pulses of patients with subclavian aneurysms.  But there is no epistemic need for this.  Here, the counterfactual version of Popper's repeatability requirement has no more epistemic merit than Popper's own repeatability requirement (2).  
   But doesn’t an effect or a piece of evidence lose its significance if someone tries and fails to replicate it?  Sometimes, but not always.  Here is an example of an effect which Claude Bernard accepted in spite of repeated failures to repeat it.  Having speculated that puncturing the fourth ventricle of an animal's heart should make the animal diabetic, Bernard tried it and got a positive result.   But the results of his next eight or ten trials were negative.  He reacted as follows.  
I found myself then in presence of a positive fact and of eight or ten negative facts; yet I never thought of denying my first positive experiment in favor of the negative experiments which followed it. Thoroughly convinced that my failures were due only to not knowing the true conditions of my first experiment I persisted in experimenting, to try to discover them.  As a result I succeeded in defining the exact place for the puncture, and showing the conditions in which the animal to be operated on should be placed; so that we can to-day reproduce artificial diabetes whenever we place ourselves in the conditions known to be necessary to its appearance.( Bernard[1949]p.173; my emphasis)
   Bernard says he never thought of denying his first result '…in favor of the [eight or ten] negative experiments which followed it'.  Far from thinking the eight or ten negative results showed that the positive result was epistemically bogus, he accepted it as the observation of a perfectly genuine effect.  Why then did he keep trying to repeat it until he learned how to reproduce the effect whenever he wished?  Apart from curiosity about his failed attempts, Bernard's motivation was practical rather than epistemic.  What he wanted was not confirmation of his first result, but rather, a technique for producing diabetic animals to experiment upon.  Continued failures (had they occurred) would  have ruled out ventricle lesioning as a practical method for this purpose.  But contrary to the received doctrine, there is no evidence that continued failure would have convinced Bernard that ventricle lesioning did not cause diabetes in his first experiment.  Bernard held that the epistemic value of an observational or experimental result depended, not on how often it occurred, but rather, on whether its cause could be found and whether, once found, it had anything of interest to teach about the physiological processes under investigation.(Bernard [1949], p.83, 178)  None of this commits him to the view that unrepeated effects or observations are illusory or otherwise epistemically defective. 
   At the very least, Bernard's story shows that not all of the best 19th century physiological research practice agrees with the received doctrine about the need for replication.  It also illustrates the distinction I drew in connection with Harvey's argument between questions about the genuineness of a putative effect or the correctness of an observation report, and questions about whether a sample of genuine effects (or correct reports) is large enough, or representative enough, to support an inductive generalization.  The results of Bernard's first trials included both a genuine (and correctly described) effect and eight or so negative results which argued against generalizing from the positive result.
	vii.	Jackson's epistemic strategy	
  To recapitulate:  Although his purposes didn't require a great deal in the way of accuracy or precision, Harvey did have to get certain details right--the difference in strength between the pulses in the swelling and the lower arm, for example.  Confident that he had the crucial details of his single case right, Harvey looked for a cause to account for them. Post-mortem observations argued that interception of blood by the aneurysm could account for the difference between the pulses, and revealed no sign of any alternative causes.  This gave Harvey a good reason to believe he had found one instance of  the effect of compressing an artery on the pulse.  Background knowledge concerning anatomical and physiological similarities in circulatory systems of various animals supported Harvey's generalizing the results of the instance he had investigated.  And the generalization provided a reason to accept the Aristotelian claim that all arteries pulsate together because their pulsation depends on the heart.
   Jackson's use of reports of partial recoveries from long term hemiplegia to confirm the claim that the same part of the body is represented in more than one motor center (A6, p.25) fits the same pattern.  He infers from reports of partial recoveries from paralysis to what he considers to be the only anatomically and physiologically possible cause.  The causal mechanism he proposes features a motor center other than the one whose loss of function caused the paralysis, which represents enough motions in the affected limb to enable the patient to regain some use of it. (Jackson [1958 II]pp.35ff.) Suppose he is right about this.  If the handful of cases Jackson considered were not anatomically or physiologically idiosyncratic with regard to the features his argument depended upon, then the recovery evidence also supports the general claim that in normal human beings a given part of the body is represented in more than one motor center.  Jackson's argument from convulsions in limbs which are temporarily paralyzed after Jacksonian seizures to the conclusion that both convulsions and paralysis can be due to loss of function in the same part of the brain (A1,p.12) follows the same pattern.  Just as Harvey began by looking for a cause for the observed differences in pulses, Jackson begins by looking for a cause for temporary post-convulsion hemiplegia.  He decides it is fatigue of corpus striatum tissue.  Just as Harvey assumes his description of the pulse pattern he observed was accurate enough for his purposes, Jackson takes it for granted that the relevant details of the few cases he considered have been described accurately and precisely enough for the purposes of his argument.  Like Harvey, he tries to show that the factor he proposes is capable of causing the effects he observed.  He doesn't mention his having tried to rule out alternative causes, but even so, his reasoning assumes that nothing other than fatigue accounts for the hemiplegia he observed.  Like Harvey, he doesn't give us an argument to show that the causal mechanism he proposed is not idiosyncratic to the patients he has observed.  But like Harvey's, Jackson's reasoning assumes that human beings are similar with regard to the features his generalization depends on.  And like Harvey, Jackson relies on observations of gross and easily identifiable effects.  A  great many of Jackson's other arguments from clinical and postmortem data employ this Harveyian strategy. 
	viii.		Replication and conditions on acceptable data
   I believe that one condition on the cogency of arguments of this sort is:
	3.	Accuracy:  The data must be sufficiently accurate and 
		precise with respect at least to all of the observational details which the 
		inference to the causal mechanism depends upon.  
What counts as sufficient depends upon what is required by the inference 
strategy.  Different  details will be relevant to different inferences.  Different degrees of accuracy will be required in different cases.  For example argument A5, p.22 above, depends upon the truth of the claim that convulsions occurred in a temporarily paralyzed limb, whose paralysis began shortly after a Jacksonian seizure.  By contrast, this argument can tolerate inaccuracies with regard to such details as the exact duration of the convulsions and their exact locations in the paralyzed limb.  On the other hand while it makes no difference to A1, p.12,  just where the Jacksonian convulsion began, the cogency of A7, p.26—the argument from the fact that Jacksonian convulsions typically begin in the hand in support of the conclusion that every term in a motor center represents motions throughout the part of the body represented by the motor center it belongs to—does depend upon where convulsions begin.  Thus an observation report which violates the accuracy condition as used in one argument, may satisfy this condition as used in another. 
   It would be hard to take Jackson's arguments very seriously if replication were the only way to find out whether this condition has been satisfied.  In many cases, his data was poorly replicated with regard to just the details his arguments depend upon.  Jackson knew his investigations were such that he could seldom hope to repeat observational results at all often. This is what he was alerting his readers to in this paper's motto (p.1), and in passages like the following:
It is most important to observe convulsive paroxysms minutely; but it is obviously difficult to observe them precisely……I never forgo an opportunity of watching patients in fits but the opportunities are rare, and the observations are painfully difficult to make.  I dare not, therefore, imply that the following is in all respects an accurate representation.  Moreover the description is admittedly incomplete.(Jackson[1958 II], p.231) 
  But the fact that replication is sometimes useful (and in some cases,  indispensable) for assessing the reliability of arguments based on empirical evidence does not prove that replicability is the cardinal and universally applicable epistemic requirement Popper and Collins took it to be.  Harvey's argument features evidence which no one would go to the trouble to repeat.  Bernard's attempts to produce diabetic rabbits shows that there can be cases in which a result is not discredited by failure to replicate.  The next sections of this paper discuss cases in which 19th century neuro-scientists considered replication to be unnecessary, and seem to have been quite right to do so because the satisfaction of the accuracy condition could be checked without replication.  
 	ix.	Assessing data without replication: evidence that speaks for itself.     
   Allan Franklin argues that some observational and experimental data are such that it would be quite unreasonable to think they could have been artifacts of the investigator's perceptual system, the way they were reported, the observational equipment used, etc.   For example some of Galileo's telescopic data exhibited regularities from which it can be calculated that the movements of Jupiter's moons come close to conforming to Kepler's harmonic law.  It is farfetched at best to think that the mechanics of Galileo's telescope could have produced as artifacts the appearances required for a principled calculation of any such precisely specified proportionality.(Franklin[1986] pp.168ff.)  It follows that given enough data to calculate the periods and the radii of the orbits of the moons, someone who knew Kepler's laws would not need to replicate the data in order to rule out the possibility of artifact due to the workings of the telescope. 
   No science comes close enough to understanding the psychological mechanisms involved in the production of the clinical and post-mortem reports Jackson used as well as physics understands the workings of a light telescope, or as well as astronomers understand the orbits of planets and moons.  Thus Franklin's argument has no strict analogues for the case of Jackson's data. But we do have enough unsystematic, rough and ready ideas about what factors can influence the production of the kinds of data Jackson worked from to support a weaker version of Franklin's argument.  It is easy to list factors which can cause misperceptions, or incomplete or inaccurate recollections or descriptions of perceptual details.  Poor eyesight, poor observation conditions (bad lighting, obstructed view, etc.) distractions, lapses in attention, lack of knowledge about what to look for and how to describe it are examples.  We know about such factors to figure out what a trained observer might overlook or describe inaccurately in circumstances like those in which Jackson and his contemporaries made their observations.  Some of Jackson's arguments are shielded from the epistemic influence of these sources of error because they do not appeal to the kinds of things trained observers would be at all likely to miss or to get wrong under the relevant conditions.  An obvious example is Jackson's appeal to reports of convulsions in temporarily paralyzed limbs.  There is next to no chance that sources of perceptual, memory, or reportorial error like those just mentioned could lead a trained observer to mistake an unconvulsed paralyzed limb for a paralyzed limb undergoing strong convulsions. As used in argument A5, p.22, this kind of evidence speaks for itself in something like the same way as the Galileo drawings Franklin discussed: we have good reason to think there are no sources of error available to distort the relevant observations in ways which would count against the arguments they figure in.  With regard to sources of error like those just considered, there is no more need to replicate Jackson evidence to see whether it is sufficiently accurate and precise for the purposes of his arguments than there would have been to replicate Galileo's drawings.	
	x.	Ruling out misdescription.
	   A skilled observer could violate accuracy condition by deliberately misdescribing an experimental or observational outcome.  Lack of descriptive abilities could lead an unskilled observer to violate the accuracy condition through inadvertent misdescription.  19th century researchers sometimes used replication to allay suspicions of these kinds.  For example, years before Walshe wrote that two cases were as good as one hundred, a British general practitioner named A.L. Wigan claimed that '…one well authenticated case  is quite as conclusive as a hundred' (Wigan [1985] p.32).  Wigan wanted to show that each cerebral hemisphere '…is a perfect instrument of thought and ratiocination' capable of operating independently of the other.(Wigan, ibid)  A single, well authenticated example of a cerebral hemisphere which actually does function acceptably well all by itself should be enough to establish this.  Nevertheless Wigan appealed to more than one case.  He feared that because he was an unknown writer who had not yet established a reputation for reliability, his own report of his own observation wouldn't be convincing.  Accordingly he cited reports made by better known investigators who had no knowledge or interest in Wigan's thesis when they made their observations.  The first case history describes 'a man of family and independence' all of whose '…mental faculties were apparently quite perfect', and whose '…mind was clear and undisturbed to within a few hours of his death'.  
On examining his skull, one [side of the] brain was entirely destroyed—gone, annihilated—and in its place (in the narrator's emphatic language) "a yawning chasm".(Wigan [1985] pp.32-33).
The second involves a gentleman
…who retained the entire possession of his faculties to the last day of his existence, yet on opening the skull, one cerebrum was reduced by absorption to a thin membrane—the whole solid contents of the one half of the cranium above the tentorium, absolutely gone.  The gentleman was subject to epileptic fits, but had no other indication of cerebral disturbance.( Wigan [1985] p.33)
Wigan sketches four more cases for good measure, but he says that provided it is well authenticated,  the first case is conclusive, and the first two are 'more than enough to show that one cerebrum is alone sufficient as an organ of thought' (Wigan [1985] p.33) 
   Wigan did not include these additional reports because he believed that unreplicated effects or observations are unscientific, or otherwise epistemically defective.  To the contrary, he said that a single well authenticated case would establish his claim that one cerebral hemisphere can support all of the mental functions.  His reason for including the additional reports was that they came from investigators  who—unlike himself—had good and widely recognized track records for honesty, observational skill, and descriptive ability.  Their reports were authenticated by their credentials as reliable observers and reporters.  Wigan did not need repeated instances of people who functioned normally with a single hemisphere intact.  As he said, all he required was a single report which his readers would have good reason to accept as epistemically good evidence for the claim he was arguing for.
  Well established investigators did not need replications to convince their readers that they were describing their observations honestly and accurately.  The writings of mid to late 19th century British neuroscientists contain disputes over many issues having to do with experimental design and  technique, methods of observation, interpretations of data, and arguments from their interpretations.  But investigators who studied the kinds of things Jackson studied, who published in the same journals, worked in the same institutions, and who belonged to the same professional groups tended to take each others' veracity and descriptive abilities for granted.  This attitude is graphically illustrated by a hostile public exchange between Marshall Hall and Robert Todd in 1848.  
   Hall had previously reported having observed that the paralyzed arm or leg of a hemiplegic whose condition was due to cerebral lesions responded more vigorously to electrical stimulation than its non-paralyzed counterpart on the other side of the body, and more vigorously than the limbs of  normal subjects.  At a well attended meeting of the Royal Medical and Chirurgical Society, Hall claimed that three years previously he had sent Todd a patient in whom this effect could easily be demonstrated.  He complained bitterly that Todd had gone on to attack his views in public without testing the patient.  To add insult to injury, Hall said, Todd had not even acknowledged receipt of the patient, let alone thanked him as common courtesy required.  Todd replied that although he had examined Hall’s patient, he did not check for the effect Hall reported because
[to] have thought it necessary to repeat Dr. Hall’s experiment on that particular patient would have indicated a distrust on my part, of Dr. Hall’s veracity.  Such was my opinion, and such, I should think, would be the opinion of most unprejudiced persons.(Hall [1848] p.395)     
   Todd wasn't the least bit averse to criticizing Hall whenever he thought he had grounds for doing so.  Thus it is impressive that as accusations and counter accusations were made by both sides, neither Todd nor any other party to the discussion even mentioned the possibility that Hall had misdescribed the results of his experiment.  
   This illustrates what I take to be the fact that from then until the end of the period during which Jackson published, descriptions of observations of gross, easily identified effects went unquestioned under the assumption that well trained, highly experienced, and professionally well established clinicians, physiologists, and pathologists would not deliberately or inadvertently mis-describe them.  Jackson's contemporaries assumed this about him, and for good reason.  His extensive writings leave little doubt that he reported his observations carefully and truthfully. Jackson was so visible that evidence of his professional honesty was easy to come by.  For people like Hall and Jackson  evidence of professional skill and integrity could be used to evaluate the likelihood of misdescription due to dishonesty or lack of observational or descriptive ability without replication. 
	   By contrast, reports of symptoms from the patients themselves, from relatives, well wishers, and lay witnesses are subject to errors due to malingering, exaggeration and fabrication.  Jackson acknowledges worries about these which he doesn't have about reports from medical professionals.  Sometimes, he allays his worries by considering repetitions of the same report.  For example, noting that patients whose fits begin in the foot tell him that their spasms go up the leg and down the arm, Jackson says 
I have no doubt they speak accurately, as I ask no leading questions and different patients tell the same tale.(Jackson[1958 I] p. 23)  
But repetition is not always necessary.  Commenting on single cases, Jackson mentions facts which argue against the possibility that the patient was faking his seizures.  For example, he says, the fits reported by his family were not like those which malingering boys commonly feign. And the symptoms Jackson saw resembled what his parents said had first occurred during sleep 'at the tender age of two'. (Jackson[1958 I], p.362)
   Jackson does have a number of instances of the same thing when he offers 'different patients tell me the same tale' as a reason to accept a patient's report.  But this is hardly a matter of carefully repeating an experimental or observational procedure to see if it yields the same result whenever it is properly executed as required by Popper.  There is no suggestion that constant repetition is required for the acceptability of the patient's report.  Jackson's point is  that his patient did not report anything unusual enough to warrant the kind of suspicions a report of something previously unheard of might deserve.       
   Another alternative to replication is the evaluation of a patient's report on the basis of background beliefs about its plausibility.
I have…had few opportunities of watching convulsions which, beginning in one side have reached the other.  One of my patients, whose fits began in his right ulnar fingers, said that  once, after the right side of the body had been involved, "it" went across his chest to the left arm; it went down that arm, but did not reach the fingers.  One dare not trust much to a patient's observation on such a matter; but, as a hint, it is of very great value.(Jackson[1958 I], p.103) 
By contrast, there are reports of occurrences which Jackson's background beliefs give him no reason to doubt.  For example, in case 4 (p.32) although Jackson doesn't believe the patient when she says she lost consciousness because of the severity of the pain she felt, he has no reason to doubt that the pain was severe. 	
	xi.	The problem of coincidental effects.
   Quite apart from the accuracy condition (3, p.52) the epistemic value of data also depends upon whether
	4.	Unity of effect: the data describe (or describe something indicative of) a single effect, or a systematically connected collection of effects, rather than two or more causally unrelated symptoms which occur together only by coincidence.
Symptoms which co-occur  just by coincidence need not indicate anything more than that unrelated causes may affect independently functioning parts of the body at the same time.  Jackson had no occasion to attempt the statistical analyses undertaken by Caramazza, Shallice, Farah, and others to determine whether deficits observed in brain damaged subjects co-occur by coincidence.  But he and his colleagues had to face crude, qualitative versions of the same question.  For example, in a report which Jackson considered to be extremely illuminating (Jackson [1866], p.606) William R. Sanders described a case which appeared to provide evidence for a
…connection of aphasia (loss of the cerebral faculty of speech) with right hemiplegia and lesion of the external left frontal convolution of the brain.(Sanders[1866] p.812)  
In addition to severe speech deficits, Sanders' patient suffered from weakness, and eventually, from partial paralysis in her right arm and leg.  But she also experienced pain in her left leg followed by paralysis.  Post-mortem examination revealed an extensive lesion of the left brain.(Sanders [1886] p.819)  How should these symptoms be parsed?  If they are only coincidentally connected, trying to explain them would be like trying to explain why a car with dents on its left passenger door has blue paint and needs gas.  Sanders and Jackson believed the speech difficulties and right side paralysis were systematically connected, and took their co--occurrence in a patient with a left brain lesion to provide evidence that the speech centers are located in the left side of the brain near motor centers for the right arm.  By contrast they thought the occurrence of the left leg symptoms was a coincidence which did not argue for anatomical or physiological connections between speech and left leg sensory or motor functions. 
   Repeated instances of similar combinations of speech, right side motor disorder and left side brain lesions without left leg pain, weakness or paralysis, would make it plausible that Sanders' patient's symptoms occurred together by coincidence.  Repeated instances of the combination of symptoms Sanders observed would argue against coincidence.  Sanders was able to support his parsing without replication.  He found a femoral artery blood clot which could operate quite independently of his patient's  brain lesions to produce both the pain and paralysis in the left leg by blocking its blood supply. (Sanders[1866] p.822) This doesn't show that coincidental co-occurrences of symptoms and causal factors can always be distinguished from systematic co-occurrences without replication.  What it shows is that Jackson and his colleagues sometimes had the good fortune to deal  with cases in which replication was unnecessary.
	xii.	The problem of anatomical and physiological idiosyncrasies.
   I have been arguing that as far as Jackson's research was concerned, the epistemic acceptability of observation reports and the genuineness of effects observed or inferred in one or a few instances could often be evaluated without replication.  This is enough to show that the received doctrine is not generally correct. It shows that in this case at least, Popper is wrong to think  that replication is necessary for intersubjective evaluations of evidence, that coincidental co-occurrences cannot be distinguished from systematically connected effects without replication, and  that only replicable observations, data, or effects are 'scientifically significant'.  And it shows that in this case at least, Collins was wrong to think that only replicated evidence can lead to substantial conceptual change among scientists.   
   But the received doctrine may seem to regain some plausibility from the consideration of a further condition on the epistemic adequacy of a Harveyian argument.  Generalizations from one or a few cases will be suspect unless 
	5.	No Idiosyncrasy Requirement:  Features of the data the generalizing argument depends on are not due (in ways which would invalidate the argument) to anatomical or physiological factors which are idiosyncratic to the individual case(s) examined.
   The possibility of meeting this condition depends in part upon a widely held assumption which Bernard articulated  as follows:
	6.	Bernard's uniformity assumption:  In physiology, a given organ always works through one and the same mechanism;…when the phenomenon occurs in a different environment, the function takes on a different aspect; but fundamentally its character remains the same.(Bernard [1949], p.47)
Few of the individual findings which interested Jackson and his contemporaries could be generalized in any interesting way if, contrary to Bernard, functionally significant parts of the CNS carry out significantly different motor or sensory functions in different normal members of the same species.
   Anyone who pursued the kind of research Jackson conducted would have to reject this possibility for reasons analogous to those Aristotle gave to explain why natural scientists should ignore Parmenides' idea that contrary to all appearances, nothing moves or changes.(Cp. Aristotle, Physics, I/iii)  Just as there would be nothing for the physicist to study if Parmenides was right and nothing moves or changes, there would be nothing for Jackson or his colleagues to study if Bernard's uniformity assumption did not hold for the nervous system.  And just as there is too much evidence of motion and change for a natural scientist (as opposed, perhaps, to a philosopher) to take Parmenides seriously, there is too much evidence in support of uniformity to make it reasonable for a physiologist to worry about violations of Bernard's assumption unless she uncovers convincing evidence against it.  This accounts for the fact that uniformity is taken for granted, not only by Jackson, but by theorists on all sides of the locationist debate ranging from Flourens and Goltz (who thought any sufficiently large bit of cerebral tissue could do pretty much the same things as any other in the same region of the brain), to more moderate anti-locationists (like Brown-Sequard, Lewes, and Jackson and his followers), to extreme locationists (like Gall and his followers).  All of them took it for granted that the brain divides into units which have the same functional capacities in all normal members of the species. In the research tradition Jackson belongs to, this assumption is so deeply rooted that it is as hard to find investigators who explicitly state and argue for it as it is to find investigators who fail to adhere to it.     
   Misclassifications of anatomical structures can lead to apparent counterexamples to Bernard's uniformity principle.  What is assumed to be a single neural organ may consist of more than one functional part, or may be a subpart of more than one functional part of the brain.  Some apparent counterexamples to Bernard's principle may be due to analogous misclassifications of functions.  But barring such mistakes, Jackson and his colleagues proceed as though it literally goes without saying that any anatomically discrete part of the CNS which performs a particular function in any normal individual can be counted on to be able to do the same job in all normal members of the same species.
   If Bernard was right, then unless the investigator has the misfortune to have unwittingly studied only atypical individuals, what he finds with regard to the physiological, anatomical, and psychological features of one or a few of his subjects will hold for normal members of the species.  Indeed--as in the case for Majendie's discovery that he could irritate  the ventral spinal roots of a few experimental animals without producing any sensory effects--what is true of a few members of one species may hold for the members of other species as well. 
   But even if Bernardian uniformity holds for the CNS of most, (or of normal, or of healthy) individuals, this assumption might be violated by atypical individuals.  This makes it reasonable to wonder whether Jackson's evidence could have derived from subjects whose structural or functional idiosyncrasies made it unsuitable as a basis for inferences to general conclusions about the normal brain.  For example argument A5 (p.22) depends upon instances of convulsions in the paralyzed limbs of long term hemiplegics.  Even though replication was not necessary to establish the occurrence of those convulsions, it doesn't follow from this that the relevant anatomical and physiological features of the patients he observed are typical enough to support generalizations which extend to other individuals.  The same can be said with regard to the argument A7, p.26, which appeals to the locations where Jacksonian fits typically begin to support the claim that no two terms represent the same part of the body in the same way.  Here you don't have to think replication is needed to validate specific observations in order to wonder whether Jackson's evidence warranted the claim that Jacksonian
…fits beginning in the hand are common, fits beginning in the cheek and tongue are less frequent, fits beginning in the foot are rare….again, taking numbers of cases, the fits which begin in the hand begin usually in the index finger and thumb; fits which begin in the foot begin usually in the great toe.(Jackson[1958 I], p.10); my italics)
With regard to Jackson's second argument (A9, p.28) from the recovery of motions after long term paralysis in support off the claim that no two motor centers represent the same part of the body in the same way, it is natural to wonder whether Jackson's sample was large enough to entitle him to conclude that in all or most of the cases in which long term hemiplegics recover some control over their limbs, the restored motions are not exactly the same as the ones that were lost.  But this is by no means to be confused with the question whether replication was necessary to establish that the restored motions differed from the lost motions they replaced in the patients belonging to Jackson's sample.
   Different strategies for deciding whether observed individuals are anatomically or physiologically atypical in ways which would invalidate the investigator's generalizations will be required in different cases.  It would not be at all surprising if some of them involved replication.  But as the epistemic value of Harvey's unreplicated observation shows, it would be a mistake to conclude that replication of the very observational data, or the effects detected from observations in one or a few cases is necessary to establish their epistemic legitimacy.  
   A friend of the received doctrine could still ask, once we have accepted Jackson's evidence, whether it is reasonable to generalize from it without repeating  it.  I have no general answer to this question. It's hard to see how A7 could be made convincing without a large sample to argue from, even though it isn't obvious that that sample would have to meet Popper's requirement of repeatability.  It's easier to see how replication could be dispensed with in connection with Jackson's recovery data (A6, p.25, A9, p.28).  Here, worries about idiosyncrasy could be allayed by anatomical and physiological considerations which do not require replications of the  recovery data.  For example, Jackson could have helped himself to evidence that it is physiologically impossible for nerve tissue which has lost its function for reasons other than fatigue to regain the ability to cause normal muscular contractions or extensions.  It would bolster his generalization to appeal to evidence that where some of the motor nerves which innervate a small bundle of muscle fibers lose their functions, the nerves which remain intact will not be able to operate the muscle fibers in a normal way.  Such anatomical and physiological considerations make it reasonable to think that normal muscle functions cannot be completely regained once the relevant neural tissue has been permanently lesioned, and therefore, that the patients Jackson observed were not atypical in failing to recover completely from paralysis or weakness.  And in this and other cases, independent confirmation from animal experiments might be brought to bear in support of a generalization. 
   Quite apart from all of this, even where replication is necessary to provide a good enough sample to mount a convincing inductive generalization, it needn't be required to establish the epistemic value of any given member of the sample.  Thus I believe that neither the need for inductively adequate samples to support general claims about the human CNS, nor the problem of idiosyncrasies save the received doctrine of replication from the counterexamples of Jackson's research.
	xiii.	An exercise for the reader.
   In discussion of an earlier version of this paper, Brian Skyrms said that although he understood cases in which it is reasonable to be satisfied by a single instance, and cases in which it is reasonable to require one hundred , he didn't know what to say about requiring two.  If what I've said shows that the acceptability of observational evidence or the genuineness of an effect can be supported without replication in any of the cases in which Jackson based arguments on just a few instances, why doesn't it show that a single instance would have been enough?  Why should Walshe have  mentioned two instances instead of just one?  The answer to such questions may turn on rhetorical factors which aren't epistemically interesting, but I have no reason to think that that's all there is to it.  The apparent preferability  of just a few instances to a single instance in 19th century brain research is a puzzle which I recommend to the reader. 
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