J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.39.9.877 on 1 September 1976. Downloaded from

Journal ofNeurology, Neurosurgery, and Psychiatry, 1976, 39, 877-884

Pure motor hemiplegia, medullary pyramid lesion, and olivary hypertrophy

J. E. LEESTMA' AND A. NORONHA From the Departments ofPathology and Neurology, Northwestern University School ofMedicine, Chicago, Illinois, USA

SYNOPSIS The case is presented of a 60 years old man who developed sudden right hemiplegia without other accompanying neurological signs and later a spastic . Neuropathological studies indicated an ischaemic lesion ofthe left medullary pyramid which was accompanied by hyper- trophy of the left inferior olivary . An additional lesion, demyelination of the right gracile tract, is poorly explained. This case represents the second reported instance of pure motor hemiplegia due to a circumscribed lesion in the medullary pyramid and possibly an unique instance of olivary

hypertrophy without obvious damage to the central tegmental tract, ipsilateral superior cerebellar guest. Protected by copyright. peduncle, or contralateral . The olivary hypertrophy is thought to have arisen from local damage to the termination ofthe central tegmental fibres at the left . The question of the development of spasticity in a pure pyramidal tract lesion is discussed.

Fisher and Curry (1965) defined pure motor consciousness, headache, convulsion, paraesthesiae, hemiplegia as a paralysis, complete or incomplete, vertigo, diplopia, dysphagia, or visual difficulty. One of the face, arm, and leg on one side unaccom- month before this episode hypertension was noted for panied by sensory signs, visual field defect, the first time. He was in congestive failure and was treated with methyldopa, digoxin and frusemide. dysphasia, or apractagnosia. In their cases that There was no previous history of transient ischaemic came to necropsy the syndrome resulted from episodes. At the time of examination he was alert, infarction in the or the basis oriented, and there was no mental impairment. The pontis. They stated that it was doubtful that a visual fields were intact; the pupils were equal and pyramidal infarction would result in pure motor reacted to light and accommodation. The extraocular hemiplegia without other medullary signs. movements were normal and there was no nystagmus. Chokroverty et al. (1975a) reported the first case Facial sensation was normal. There was a question- of an infarction of the medullary pyramid in able mild right central facial paresis; there was which hemiplegia was the only sign. We report flattening of the right nasolabial fold but no deviation http://jnnp.bmj.com/ another case of motor due to an of the angle of the mouth. No dysphagia, palatal or pure hemiplegia lingual paresis, or palatal myoclonus was noted. The ischaemic vascular lesion of the medullary patient had a right hemiplegia which was dense in the pyramid. arm, less in the right leg with the muscle strength estimated at 4/5. Initially there was flaccidity in the CASE REPORT hemiplegic limb but in two weeks this changed to spasticity on the affected side. The were A 60 years old man developed weakness of the right brisker on the affected side and right ankle clonus was on September 26, 2021 by side of his body on 2 November 1973. The onset of also noted. The plantar responses were extensor on weakness was sudden. There was no impairment of the right and flexor on the left. There were no cerebel- lar signs, no sensory deficit to touch, pin-prick, vibration, orjoint position. Cortical sensory functions I Address for correspondence and reprimt requests: Dr Leestma, were intact. There were bilateral carotid bruits. A Department of Pathology, Northwestern University School of Medicine, 303 East Chicago Avenue, Chicago, Illinois 60611, USA. scan performed two weeks after admission was (Accepted 26 April 1976.) interpreted as within normal limits. 877 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.39.9.877 on 1 September 1976. Downloaded from

878 J. E. Leestma and A. Noronha

The patient was discharged three months later appeared altered and was substantially larger and with improvement in the hemiparesis. He was re- more distinct than the right. These changes in the admitted in September 1974 with gangrene of the olive were seen throughout the medulla. The speci- lower right leg. An aortogram revealed occlusive men terminated at the lower medullary level and no vascular disease with complete obstruction of the was available for study. Sections of the right femoral . An above the knee amputation revealed no abnormality, the dentate was done and the patient recovered promptly. He was nuclei appearing well preserved. admitted again in October of 1975 for an inguinal Microscopically, sections stained with haematoxy- herniorrhaphy. After this procedure he sustained a lin and eosin, and Kluver-Barrera stain (Nissl with cardiac arrest and after abortive resuscitation he died. Luxol Fast Blue) were studied. The sections correlated well with the gross findings. The was NECROPSY FINDINGS The general necropsy revealed unremarkable. One or two senile plaques were found severe atherosclerosis which involved , carotid only in the hippocampus. The small lacunar infarcts , coronary arteries, and peripheral vessels in in the were all old and the sections of the extremities. There was a massive acute myocardial mid-brain and showed no lesions and uniform infarction affecting the posterior wall of the left myelinization. The most rostral section of the medul- ventricle with evidence of old scarring and hyper- lary region (Fig. I) showed myelin loss in the left trophy throughout the left ventricular myocardium. pyramid extending to a small extent into the medial There was an unruptured abdominal aortic . lemniscus. There was also some pallor in the myelin Pulmonary oedema and congestion were noted as of the external arcuate fibres lateral to the left olive. were other signs of terminal myocardial failure. The The olive itself showed no alterations apart from the stump of the right leg was well healed. usual accumulation of lipofuscin within the neurones guest. Protected by copyright. at this level. There was pronounced astrocytosis in NEUROPATHOLOGICAL EXAMINATION Grossly, the the affected pyramid as well as a slight perivascular brain was unremarkable; no obvious lesions pre- lymphoid cell infiltrate. Scattered lipid laden macro- sented themselves. The leptomeninges were slightly phages as well as some swollen axons were seen in the thickened in keeping with the age of the patient and pyramid. The opposite pyramid was unremarkable. slight cortical atrophy mostly in the frontal lobes was In the mid-portion of the medulla at the level of the present. The inferior surface of the brain revealed no 12th cranial nucleus (Fig. 2) several changes obvious abnormalities with the circle of Willis con- taining only scattered atheromatous plaques, signi- cantly less in amount than were seen in the extra- cranial vessels. The plaques were found mostly in the internal carotid vessels, scattered along the middle cerebral arteries, at the distal ends of the vertebral arteries and at the proximal and distal ends of the basilar artery. The circle of Willis was normal anatomically with two vertebral arteries of about equal calibre, two posterior communicating and one anterior communicating artery. No obstruction ofany vessel was noted. Outwardly the brain stem and http://jnnp.bmj.com/ cerebellum appeared unremarkable. Multiple coronal sections of the brain revealed slight cortical atrophy with widening of the sulci and widening of the insula. The ventricles were slightly enlarged. The cortical ribbon was uniform and there were no cerebral softenings. The globus pallidus and putamen contained several small perivascular la-

cunes, but none was larger than two millimetres. The on September 26, 2021 by was preserved. Cross-sections of the mid- brain revealed a pigmented substantia nigra and a patent aqueduct and no lesions. No lesions were found FIG. 1 The most rostral section ofmedulla stained by in the pons. However, the most rostral section of the the Kiiver-Barrera methodshows myelin loss in the left revealed that the left medullary pyramid as well as slight pallor laterally and medially. pyramid was shrunken and of a tan-brown colour No hypertrophic changes in the inferior olives at this compared with the right. The inferior olive also level are noted. J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.39.9.877 on 1 September 1976. Downloaded from

Plure m0otor hemiplegia, medullary pyramid lesion, and olivary htypertrophy 879

( FIG. 2 A mid-sectioni of the mnedulla reveals the same FIG. 3 The most caudal section of medulla illustrates pyramidal mnyelin loss as in Fig. 1 but additionally the continued pyramidal tract demyelination, hyper- shows hypertrophic changes in the left inferior olivary trophy ofsuch olivary elements as are remaining on the nucleus. Myelin pallor lateral and medial to the olive left side, and myelin loss in the right gracile nucleus and guest. Protected by copyright. is also noted. tract.

were apparent. In addition to the changes previously alterations in the left medullary pyramid; hyper- noted in the pyramid, there was pronounced hyper- trophy of the caudal half of the left inferior olivary trophy of the left inferior olivary complex. The olivary nucleus; myelin loss in the right gracile tract. neurones were generally swollen, pale, and contained numerous clear vacucles with only occasional cells appearing shrunken and pyknotic. Astrocytosis was DISCUSSION also present. In some neurones the cytoplasm appeared to be refractile and what Nissl substance The clinical features in our patient are consistent could be found was compressed into dark specks. The with the definition of pure motor hemiplegia as opposite olivary nucleus was normal in appearance described by Fisher and Curry (1965) and similar as were the 12th nerve nuclei and other dorsal nuclear to such a case as reported by Chokroverty et al. masses. (1975a,b). A review of the supply to the A section of the caudal medulla (Fig. 3) revealed, in medulla oblongata is necessary to appreciate the addition to the previously observed changes of the possible pathogenesis of the pyramidal and pyramid and olive, that the right gracile tract had lost http://jnnp.bmj.com/ substantial amounts of myelin. Neurones in this olivary lesions. region were preserved but there were numerous The first comprehensive work on the blood spheroids, mineralized concretions, and astrocytosis. supply of the brain stem is the work of Stopford With the exception of the myelin loss these same (1916a,b,c). Later investigations on the subject changes were seen in the opposite gracile tract and added only slightly to his observations (Foix and nucleus. The cuneate nucleus showed similar dys- Hillemand, 1925; Krayenbiuhl and Yasargil, trophic changes. There was no inflammatory or 1957). From a review of Stopford's work and phagocytic activity in the right gracile tract and examination of several specimens of our own, it is on September 26, 2021 by nucleus. apparent that the blood supply of the medulla is Histological examination of the cerebellum in- 4 illustrates the cluding the dentate nuclei revealed no changes apart complex and variable. Figure from hypoxic alterations which were interpreted as blood supply of the ventral medulla. As Foix and agonal. Hillemand (1925) pointed out there are medial The outstanding neuropathological findings in this (paramedian), short and long lateral vessels which patient which deserve comment are: degenerative arise from the vertebral and anterior spinal J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.39.9.877 on 1 September 1976. Downloaded from

880 J. E. Leestiia and A. Noronha

VERTEBRAL ART. ANT. SPINAL ART. guest. Protected by copyright.

FIG. 4 The vascular supply ofthe inedtulla. Two verte- bral arteries (VERT) join to form the basilar artery (BAS) giving off two major branches, the posterior inferior cerebellar arteries (PICA) and the anterior inferior cerebellar arteries (AICA). Finer branches, most of which penetrate the mwidline to suipply the pyramids andadjacent structutres, occur in threegeneral groups: (1) those arising from the tipper vertebral arteries, (2) those wt'hich arise at the origin or tipper portion of the (s) (ASA), and (3) FIG. 5 The territories of siupply of the vertebral those which arise more cauidally along the anterior arterial branches and the small branches ofthe anterior spinal artery where it is a single vessel. spinal artery in the medulla. The supply ofthe posterior inferior cerebellar artery and its branch, the are not shown but suipply the remaining unshaded or lnspotted regions (after Stopford, http://jnnp.bmj.com/ 1916a,b). arteries which supply the ventral and lateral medulla. The rostral median branches arise from the and penetrate the midline between the pyramids, there to ramify and supply the pyramid, medial portion of the olive, medial posterior inferior cerebellar artery. At this most

lemniscus, and other structures which include the rostral level, the junction between pons and on September 26, 2021 by floor of the and the cranial nerve medulla, there is usually no circulatory con- nuclei dorsally near the midline as depicted in tribution made by the anterior spinal artery. At Fig. 5. Other more lateral branches supply lateral mid-medullary levels a narrow territory is sup- medulla and leaving the resti- plied by the vertebral artery which runs from the form body (inferior cerebellar peduncle) and region lateral to the dorsal motor nucleus of the to be supplied by branches ofthe vagus through the inferior olive laterally. The J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.39.9.877 on 1 September 1976. Downloaded from

Pure motor hemiplegia, medullary pyramid lesion, and olivary hypertrophy 881 remaining ventral and midline structures are medulla most probably represents a descending supplied by similar median and short lateral degeneration which, if the spinal cord had been branches of vessels arising from the anterior available for study, would have shown a continu- spinal artery as shown in the same figure. More ation of the degeneration downward into the right dorsal structures are supplied by the posterior . The inflammatory infiltrate spinal artery and branches ofthe posterior inferior and persistent macrophage response is typical for cerebellar artery. old infarctive or ischaemic lesions and in de- In the caudal medulla, anterior spinal artery generating tracts. There is no suggestion in the branches supply the pyramid and median struc- material or in the rest of the case to suggest an tures as well as some ventral lateral regions. There inflammatory or infectious aetiology for the brain is some territorial overlap between the more stem pathology. lateral supply of the vertebral arterial branches and the posterior spinal artery territory. It is FUNCTIONAL IMPLICATIONS OF PYRAMIDAL LESION possible that a 'watershed zone' exists in the According to classical concepts, in a pyramidal region jointly supplied by small vessels arising tract lesion one expects to observe a spastic from the vertebral artery and those ofthe anterior (hypertonic) paralysis of the affected extremity spinal artery at upper-mid medullary levels. The after the immediate period ofneural shock abates; existence of such a 'watershed' might be important however, it appears that when neurosurgical to the pathogenesis of ischaemic lesions in this interruption of the pyramidal tract in man or in region such as the case reported above. monkeys occurs the opposite is observed, or, at guest. Protected by copyright. best, variable results have been obtained (Beck PYRAMIDAL LESION A discrete lesion as described and Chambers, 1970; Gilman and Marco, 1971). above is unusual but has been described in one In the few studies involving man, most notably recent report (Chokroverty et al., 1 975a) and in at the report of Bucy et al. (1964) where the pyra- least two previous reports in the older literature. midal tract was interrupted at the level of the One of these was probably of atherosclerotic , after a period of recovery the origin in which the lower medulla at the level of patient moved quite well with no important signs the pyramidal was affected by a dis- of hypertonia with the possible exception of crete lesion (Stopford, 1916c), and another in Babinski's sign in the affected lower extremity. It which syphilitic vasculitis most probably resulted appears then that pure lesions of the pyramidal in ischaemia of the pyramid and adjacent struc- tract do not produce a spastic type of paralysis in tures, much as in our case except that there is no man or in the monkey. The present case must be suggestion of syphilis in the present patient somewhat ofa rarity in this respect as a ratherpure (Lhermitte and Trelles, 1933). In this latter case, lesion seems to be present in the medullary pyra- the pyramidal lesion was accompanied by olivary mid and yet the patient suffered many of the hypertrophy. We surmise that some impairment accepted signs (Landau, 1969) of a hypertonic of circulation to the left pyramid of our patient paralysis. A re-examination of the other reports occurred in 1973 which may have been in the form of similar discrete lesions in the medulla in man http://jnnp.bmj.com/ of a migrating thromboembolus, in situ thrombo- (Chokroverty and Rubino, 1 975a,b) indicates sis, hypotensive episode, or all three. The area de- that in these cases thepatients' affected extremities prived of blood supply was in the territory served were more hypotonic than hypertonic, though by the medial penetrating branches of either the some slight increase in tonicity and a Babinski's vertebral or anterior spinal arteries ofthe left side. sign was observed. Admittedly, a detailed clinical It is likely that a long-standing total occlusion did observation was not available on our patient, but not occur, for ifit had, the result would have been from the records available to us many of the on September 26, 2021 by a cavitary lesion of larger proportions probably criteria for spasticity were met. not limited to the small area observed in this case. Why then in the face of other human material In addition, there would have been more exten- of a similar type where hypotonicity or the lack of sive neuronal damage than was observed here hypertonic signs were noted does our case where arcuate nuclei were preserved and the olive exhibit signs of spasticity? Several possibilities was still viable. The myelin loss below the rostral exist, but a complete exploration of them, the J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.39.9.877 on 1 September 1976. Downloaded from

882 J. E. Leestma and A. Noronha neuroanatomical and neurophysiological con- superior cerebellar peduncle can similarly pro- troversies which are involved in the question of duce the lesion on the ipsilateral olive (Vuia and the mechanism for spasticity, and the anatomy of Rothemund, 1971). It appears that this unusual the pyramidal tract and its function are beyond the reaction on the part of the olive results from scope of this paper. significant deafferentation at some distance from Briefly, however, it is possible that anatomical it or by lesions in its immediate vicinity (Aberfeld, variations played a part in the development of 1966). Interruption of efferent olivary fibres is symptoms in this man as it is known that con- not known to produce hypertrophy but induces siderable variations exist in the anatomy of the atrophy (Aberfeld, 1966; Sohn and Levine, 1971). pyramidal tract in man (Nyberg-Hansen and The anatomical connections of the inferior Rinvik, 1963). It could be that most of this man's olivary nuclei in man are based on relatively few motor connections with the spinal cord were studies with most data having been extrapolated interrupted by the lesion, with virtually no con- from studies in cat and to a lesser extent from tribution from the opposite pyramidal tract monkey and other animals. In this system such existing. This lesion is quite distinct but there is animal studies probably have only limited rele- some extension into the medial leminiscus not to vance to man (Scheibel and Scheibel, 1955), as mention the obvious involvement of the inferior pathways demonstrated by many workers in cats olive on the left side and the myelin loss in the projecting to the olives have not been sub- gracile tract on the right side (which is poorly stantiated in man (Verhaart and Voogd, 1962; explained). It is possible that these lesions might Lapresle and BenHamida, 1970). guest. Protected by copyright. further contribute to the already heavily de- The inferior olive in man probably receives afferented motor horn, thus releasing it to local input from a number of sources both above and influences which are said to be the basis for below it, but the major contribution comes from spasticity in instances such as spinal cord injury the contralateral dentate nucleus of the cere- where more than simple motor interruption bellum passing into the brain stem by way of the occurs (Bucy et al., 1964; Dimitrijevic and brachium conjunctivum (superior cerebellar pe- Nathan, 1967; Landau, 1969; Gilman and duncle) probably collecting some fibres from the Marco, 1971). This hypothesis is further strength- or its vicinity and crossing the midline ened by the recent report of Chokroverty within the commissure ofWernekink at that level. (Chokroverty and Rubino, 1975b) that in such From here the fibres descend within the central discrete pyramidal lesions as our case there may tegmental tract to enter the inferior olive over a be subtle sensory dysfunction as well. broad front superiorly and laterally (Gautier and Blackwood, 1961; Verhaart and Voogd, 1962; OLIVARY LESION The subject of olivary hyper- Crosby et al., 1962; Lapresle and BenHamida, trophy has been studied for many years with 1970). There is a rich intercommunication several reports antedating the turn ofthe century. between the olives on both sides by means of a These older references can be found in a recent mass of crossing fibres which pass through the article (Horoupian and Wisniewski, 1971). Since (Scheibel and Scheibel, 1955; http://jnnp.bmj.com/ that time several reports have dealt with the Crosby et al., 1962). phenomenon itself and in relation to palatal Output from the olivary nuclei also varies in myoclonus which sometimes occurs with olivary many respects from species to species but the hypertrophy (Marie and Foix, 1913; Lhermitte major outflow in man is probably to the cerebellar and Trelles, 1933; Davison et al., 1936; Gautier cortex with lesser connections going to the nearby and Blackwood, 1961; Aberfeld, 1966; Lapresle reticular formation and to the spinal cord and BenHamida, 1970; Sohn and Levine, 1971). (Holmes and Stewart, 1908; Crosby et al., 1962). on September 26, 2021 by From these accounts it is apparent that olivary From an examination of Fig. I it is evident at hypertrophy can occur when there are inter- the highest medullary level shown that there is ruptions of the ipsilateral central tegmental tract, some myelin loss laterally in the external arcuate or when this tract is intact but when the contra- fibres ofthe left olive, though there are no changes lateral dentate nucleus in the cerebellum has been of olivary hypertrophy at this level. Likewise, destroyed or its fibres interrupted. Lesions of the there is pallor in the region between the two J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.39.9.877 on 1 September 1976. Downloaded from

Pure motor hemiplegia, medullary pyramid lesion, and olivary hypertrophy 883 olivary nuclei. Similar changes, though more do not resemble those of an infarct or ischaemic developed, are noted in the mid-section of the lesion, though this latter possibility should be medulla in Fig. 2. Here the hypertrophic changes considered. Other changes in the gracile and are quite distinct. The question now arises, what cuneate nuclei of the caudal medulla include is the cause for the hypertrophic change ob- spheroids, mineralized concretions, and gliosis served? The most satisfactory explanation is that which can be regarded as accompaniments of the the central tegmental fibres which entered the left aging process as documented by others (Brannon olive by way of the external arcuate bundle were et al., 1967). The fact that there were no clinical damaged by the ischaemic process in the region, signs of sensory disturbance (touch and position) with damage most severe in the lower portion of on the right side in view of some myelin loss in the the medulla. Since tegmental fibres appear to be right inferior medial lemniscus is also curious. the most important for maintenance of the olive, This region would have been expected to produce a large number of these fibres at the lower level some impairment of these sensory modalities in must have been interrupted. It is likely that many the right leg (Crosby et al., 1962) due to somato- decussating fibres were also damaged by the topic localizations in the medial lemniscus. It is lesion but these must have been of lesser impor- possible that, with the severe peripheral vascular tance to the opposite olive as no changes of disease present, this relatively subtle change was hypertrophy or neuronal reaction were noted not appreciated. On the other hand it is possible there. Such regional lesions are thought to be that the medullary lesion had not yet expanded at important to the development of hypertrophy as the time of the careful neurological examination guest. Protected by copyright. has been pointed out by Aberfeld (1966). into that area to cause symptoms or signs. Later The cellular alterations in the neurones of the on, with the amputation all chances of docu- left olive consisting of swelling, chromatolysis, menting such a possible deficit were lost with the vacuolation, occasional shrinkage, and fila- leg. That subtle sensory deficits can occur in cases mentous hypertrophy are typical and have been of pure motor hemiplegia and be clinically described elsewhere (Lhermitte and Trelles, 1933; unnoted is described in a recent publication by Gautier and Blackwood, 1961; Horoupian and Chokroverty and Rubino (Chokroverty and Wisn ewski, 1971; Sohn and Levine, 1971). A Rubino, 1975b). unique feature illustrated in this case is that hyper- This case represents an unusual combination of trophy of the olive can arise from a local lesion clinical and anatomical problems which may be and not by a major lesion rostral to it as is usually unique. It further illustrates the value but frustra- the case. tion inherent in human neurological material in The absence ofpalatal myoclonus is frustrating that, had the character of the lesion been appreci- but its absence in the presence ofknown lesions of ated sooner, more elegant neuroanatomical the central tegmental tract with and without techniques might have been applied and more olivary hypertrophy has been noted, though might have been learned from the unusual lesions unexplained, by others (Lhermitte and Trelles, in this case. http://jnnp.bmj.com/ 1933; Davison et al., 1936). From an anatomical point of view this problem is a nagging one and only further experimental work will resolve this REFERENCES enigma. Aberfeld, D. C. (1966). The hypertrophic degeneration of the olives. Acta Neurologica Scandinavica, 42, 296-306. GRACILE TRACT DEMYELINATION We are at a loss Beck, C. H., and Chambers, W. W. (1970). Speed, accuracy to explain adequately the myelin loss in this tract and strength of forelimb movement after unilateral and nucleus on the right. The high leg amputation pyramidotomy in rhesus monkeys. Journal of Coin- on September 26, 2021 by accomplished several months before death parahiie and Physiological Psychology, 70, 1-22. ablated some sensory output into the ipsilateral Brannon, W., McCormick, W., and Lampert, P. W. (1967). Axonal dystrophy in the gracile nucleus of man. Acta gracile tract but, in the absence of either a root or Neuropathologica, 9, 1-6. lesion, ascending degenera- Bucy, P. C., Keplinger, J. E., and Siqueira, E. B. (1964). tion would ordinarily not be expected (Norton, DestruLction of the 'pyramidal tract' in man. Jouirizal of 1969). The changes seen in the tract and nucleus Neurosurgery, 21, 385-398. J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.39.9.877 on 1 September 1976. Downloaded from

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