Journal of Neurology, Neurosurgery, and Psychiatry 1986;49:686-694 Unilateral left paramedian infarction of thalamus and midbrain: a clinico-pathological study J BOGOUSSLAVSKY,* J MIKLOSSY,t JP DERUAZ,t F REGLI,* G ASSAL$ From the Department of Neurology,* Division of Neuropathology,t and Centre of Neuropsychology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland SUMMARY In a patient with a unilateral embolic infarct in the left posterior thalamo-subthalamic paramedian artery territory, neuropathological studies showed involvement of the intralaminar, dorsomedial, and internal part of the ventral posterior nuclei of the thalamus, of the rostral part of the mesencephalic reticular formation, and of the posterior commissure. The patient showed upgaze palsy for voluntary saccades, smooth pursuit and vestibulo-ocular movements, sustained downgaze, right-sided motor hemineglect and facio-brachial hypaesthesia, motor transcortical aphasia and anterograde amnesia. This case confirms that unilateral destruction of the posterior commissure, rostral interstitial nucleus of the MLF and interstitial nucleus of Cajal produces a non-dissociated upgaze palsy. Involvement of the nucleus of Cajal probably produced the sustained downward deviation of the eye, by causing predominance of downward vestibulo-ocular inputs. This case also shows that thalamic aphasia and anterograde amnesia may be related to a paramedian lesion of the thalamus, with special reference to involvement of the dorsomedial nucleus, in the absence of lesion of the pulvinar and mamillo-thalamic tract and of conspicuous involvement of the ventral lateral nucleus. Selective hemineglect for motor tasks may occur in infarction of the dominant thalamus, involving the intralaminar nuclei. Unilateral infarct of the thalamus and/or midbrain is unusual and pathologically proven cases are uncommon in the literature.' 13 In these reports, clinical data are often lacking and in many cases, it is difficult to establish clinico-anatomic correlations. We have studied a patient with complex disturbances of vertical movements and neuropsychological impairment, who died 2 weeks after onset of the symptoms. At necropsy, there was a recent unilateral infarct involving the paramedian part of the thalamus and upper midbrain on the left side. Case report A 72-year-old right-handed housewife was admitted after she suddenly experienced right-sided weakness and speech disturbances. Seven years before, she had a right mammectomy for a breast cancer, and 6 months before admission she suffered an inferolateral myocardial infarct. On admission, the patient was slightly drowsy, disorientated in time Address for reprint requests: J Bogousslavsky, Service de Neurologie, CHUV, 101 I Lausanne, Switzerland. Received 26 February 1985 and in revised form 12 August 1985. Accepted 25 August 1985 and place, and showed the speech disturbances described below. On cranial nerves examination, except the oculomotor disturbances, the patient showed tactile and thermo-algesic hypaesthesia of the right side of the face, and a moderate right central facial paresis. The visual fields were complete, with no visual neglect on simultaneous presentation of visual stimuli in the temporal fields. A slight proximal paresis of the right upper and lower limbs was present, without hyperactive tendon reflexes or Babinski's sign. The patient did not spontaneously use her limbs on the right side, although she could move them perfectly under sustained verbal stimulation. Withdrawal to pain was absent on that side, although the patient reported that she could feel a painful sensation (despite the slight decrease of superficial sensation in this side of the body). Also, she did not maintain the right arm extended more than 4-5 seconds, and did not adequately place this arm when resting in bed, leaving it aside in inappropriate and uncomfortable positions. A slight decrease of tactile and algesic sensation was present in the right upper limb and trunk down to DIO, without sensory extinction on simultaneous tactile stimulation of both sides of the body. Postural and vibratory sensation was normal. The gait was not evaluated. The blood pressure was 180/120 mmHg, with pulsations of 84/minute. General examination was normal. Oculomotor findings In primary position, the patient showed sustained conjugate downward deviations of the 686 687 Unilateral left paramedian infarction of thalamus and midbrain: a clinico-pathological study curring digits (maximal span: 2, failure of span + I learneyes, with a very slight inward deviation. A very slow elevation of the eyes was possible from this downward position, on voluntary and smooth pursuit movements, but with a maximal amplitude of 10°-15°. No upward saccade could be elicited. No movement was produced on vertical oculocephalic manoeuvre (with Frenzel glasses). Caloric testing not performed. Abduction of the right eye was limited on voluntary and smooth pursuit movements (with diplopia), but a full range deviation could be obtained on horizontal oculocephalic manoeuvre. Vertical optokinetic responses were abolished (optokinetic drum, 20° 40°/s). Horizontal optokinetic responses were normal. Convergence could not be elicited voluntarily or on pursuit attempts. The right pupil showed a relative miosis (1 5 mm, vs 2 mm), with weak direct and consensual reactions on both sides. These findings did not change before the patient died. Neuropsychological findings Only a partial assessment was realised, because the patient died unexpectedly 2 weeks after admission. On adnission, the patient was disorientated in time and place. Her speech was reduced, non-fluent, with frequent pauses and decreased volume of the voice. She made semantic and less often phonemic paraphasias. Repetition of words, non-words and sentences (up to 15 words) was preserved. Verbal comprehension was normal for simple orders but was impaired for complex orders (Pierre Marie's three papers). No buccolingual apraxia was noted. The motor neglect of the right upper and lower limbs has been described with the neurologic findings. Thirteen days later, the patient underwent a more detailed neuropsychological examination. She was slightly apathetic but not drowsy and she collaborated well but was still disorientated in time and place. Spontaneous speech was still reduced and the sentences were very rarely formed by more than three to four words. No echolalia was present. Verbal comprehension was good even for complex orders (Pierre Marie's three papers, Token test), but the patient frequently interrupted the execution of a task before its completion. Repetition of words (1-8 phonemes), non-words and sentences (3-15 words) was normal. Verbal automatic series (weekdays, months) were correctly realised anterogradely, but retrograde naming showed perseverations. Naming was deficient on Boston Naming test (21 correct answers/76), with either anomia or semantic paraphasias. The reading of letters was good, but the patient was unable to read a text, because of diplopia and production of semantic paralexias. She could perfectly transpose into sentences a text spelled by the examiner. Spelling showed numerous errors. The patient was not able to write or draw, because she did not initiate the movement of the right hand. Oral calculation was impossible because of difficulties in recalling the numbers. Visuo-spatial recognition was impaired (Ghent: 29 correct answers/36, Poppelreuter 1/4, inadequate geographic orientation on a map). The patient was unable to recall any events which had happened to her after the onset of her stroke, and she could not recall what she had been doing minutes, hours, or days before the examination. Events that had happened a few months or years before were adequately recalled despite the speech disturbances. Learning of series of 3-10 words was impossible: the patient recalled none or only one of the words even after five trials. Sometimes, perseveration of one word from a preceding series occurred. These marked difficulties for verbal learning were confirmed on Hebb's re- ing). A similar impairment of visual learning was also observed on Corsi's block-tapping (maximal span of 3, failure of span + I learning). During these tests, the patient remained attentive and did not show distractibility. Laboratory findings Chest radiographs, standard blood and urine tests were normal (except a thrombocytosis of 600 x 109/1). ECG showed widespread ischaemic changes and signs of the ancient inferolateral infarct. An EEG made 10 days after admission was normal, except for episodic theta waves in the left premotor region. Two CT scans showed a paramedian hypodense area in the left thalamus, with slight enhancement after intravenous injection of contrast medium, and with normal ventricular size. CSF was normal, with a pressure (lumbar) of 13 mm H20. Doppler ultra sonography with spectrum frequency analysis did not show extracranial stenosis. Somatosensory evoked potentials were normal bilaterally (median nerve stimulation). Evolution The patient was put on intravenous heparin therapy (30,000 U/24 h). After 10 days, this therapy was replaced by subcutaneous heparin (2 x 5000 U/24 h) and acetylsalicylic acid by mouth (I g/24 h). Fourteen days after admission, while resting in bed, the patient suddenly fell in deep coma, with intermittent apnea and unmeasurable blood pressure. She could not be resuscitated and died after 10 minutes. Pathological findings Necropsy showed generalised atherosclerosis, multiple recent and old myocardial infarcts without intracardiac thrombus, thrombosis of the left femoral vein, and pulmonary emboli (the probable cause of death). The liver conTable I Involvement ofthalanic and mesencephalic structures related to the symptomatology of our patient left side Ventral lateral nucleus Dorsomedial nucleus Centromedian nucleus Parafascicular nucleus Paracentral nucleus Central medial nucleus Lateral posterior nucleus Ventral posterolateral nucleus Ventral posteromedial nucleus Nucleus reuniens Subthalamic nucleus Mamillotegmental tract Zona incerta Field H of Forel Lenticular fasciculus Thalamic fasciculus Nucleus ruber Fasciculus retroflexus Central tegmental tract Medial longitudinal fasciculus Rostral interstitial nucleus of MLF Interstitial nucleus of Cajal Nucleus of Darkschewitsch Nucleus of posterior commissure Posterior commissure + +++ ++++ + +++ ++++ + +++ + + + +++ + +++ + ++ + ++ + ++ +++ + ++ + ++ ++ + +++ ++++ + (rostral part) + +++ ++ (rostral part) ++ (rostral part) + +++ + +++ right side (+) - - The number of plus signs (+) reflects the severity of the lesions. -:no lesion. 688 tained many metastases from the breast carcinoma operated 7 years before. Gross examination of the brain (weight 1230 g) showed only mild atherosclerosis of the circle of Willis. The sections of the brain showed an isolated macroscopical finding: a paramedian infarct in the left thalamus and in the subthalamic region (1,7 x 0,8 cm), extending from the level of the mamillo-thalamic tract to the periaquaeductal gray matter (fig 1). This partly haemorrhagic infarct was situated in the territory of the posterior thalamosubthalamic paramedian artery. Fragments of the brain were submitted for microscopic examination of the right central circonvolution, left central circonvolution, left inferior parietal circonvolution, left superior parietal and left supramarginal circonvolution, right parietal region, left parieto-occipital region, and medulla oblongata. The blocks were embedded in paraffin and cut at 10 gim sections. They were stained with haematoxylin-eosin, crezyl violet, Loyez and van Gieson luxol fast blue (myelin stain), Holzer stain and PTAH, van Gieson elastin, Perl's prussian blue, periodic acid Schiff, Congo Red. Blocks comprising thalami, subthalamic regions, midbrain and pons were studied in 312 serial sections and stained alternatively with haematoxylin and eosin and Loyez stain. Further frozen sections (after passage in sucrose) of blocks from the right and left pre and Bogousslavsky, Miklossy, Deruaz, Regli, Assal postcentral gyrus were stained with crezyl violet, Bodian and Glees stain (for axons) and Schroeder stain (myelin stain). Microscopic study of the left thalamo-mesencephalic infarct showed several haemosiderin-laden macrophages, astrocytic gliosis, neovessels and axonal swellings. Some small vessels within the infarct were occluded by emboli. The rostral extremity of the softening was situated at the level of the mamillo-thalamic tract, where two areas of infarction in the dorsomedial nucleus were present, without involvement of the mamillo-thalamic tract (fig 2). The infarct destroyed the medial rostral part of the cerebral peduncle and fibres of the mamillo-tegmental tract near their origin. The serial sections revealed a well delineated infarction in the dorsal part of dorsomedial nucleus, the centromedian nucleus, parafascicular, paracentral nuclei, the nucleus reuniens, the ventral posteromedial nucleus (VPM), the medial part of the ventral posterolateral nucleus (VPL), a small part of the posterior portion of the ventral lateral nucleus (VL), and a large part of the subthalamic nucleus (table 1, fig 2). More caudally the medial-rostral part of the red nucleus and the central gray matter of the third ventricle at the level of the rostral interstitial nucleus of MLF were involved. The fasciculus retroflexus and the fibres of the central tegmental tract were also destroyed, as the field H of MENENg-, A p .011 I ,1-< Vr paramedian artery. Unilateral left paramedian infarction of thalamus and midbrain: a clinico-pathological study Forel, the thalamic fascicle and fibres of the ansa lenticu- Discussion laris. Caudally, the infarct involved the left part of the posterior commissure, sparing some ventrocaudally crossing fibres. The pulvinar was not involved. The caudal end of the lesion was situated at the level of the posterior commissure (PC): the whole rostral interstitial nucleus of MLF (riMLF), the rostral half of the interstitial nucleus of Cajal (iC) and of the nucleus of Darkschewitsch (nD) were involved (fig 3), as well as the most rostral fibres of the left MLF. The oculomotor nuclei, their roots, and the remainder of the brainstem were intact. The right thalamus did not show any significant lesion (an area of focal demyelination of a few gm was demonstrated in the parafascicular nucleus). Rare minute recent infarcts measuring a few pm, probably secondary to emboli, were seen in the central region of both hemispheres. In order to detect any axonal degeneration in layer IV and a possible neuronal loss or degeneration in layer VI (the lamina of origin of most cortico-thalamic fibres) in the somatosensory cortex due to lesions in the VPM, serial sections of small tissue blocks, taken in areas 4, 3, 1 and 2 of both hemispheres, were examinated with special techniques,14 15 and showed degenerated fibres. 0 (h Fig 2 Camera lucida drawings of transverse coronal sections through the thalamus. CC = corpus callosum, c = caudate nucleus, MB = mamillary body, Mth = mamillo-thalamic tract, Mte = mamillo-tegmental tract, Lf = lenticularfascicle, III V = third ventricle, CrC = crus cerebri, AN = anterior nucleus, DM = dorsomedial nucleus, CM = centromedian nucleus, Pf = parafascicular nucleus, LD = lateral dorsal nucleus, LP = lateral posterior nucleus, VL= ventral lateral nucleus, VPL = ventralposterolateral nucleus, VPM = ventralposteromedian nucleus, Sth = subthalamic nucleus, RN = red nucleus, SN = substantia nigra, MGB = medial geniculate body, LGB = lateral geniculate body, III N = oculomotor nuclei, PC = posterior commissure. 689 The thalamo-mesencephalic infarct was related to proven emboli in the posterior thalamo-subthalamic paramedian artery. These emboli probably arose from the heart, which showed recent myocardial infarcts. The slight right-sided weakness probably corresponded to involvement of the ansa lenticularis, and the decrease of superficial sensation in the right upper part of the body down to D 10 was related to involvement of the ventral posteromedial nucleus (face) and of the internal part of the ventral posterolateral nucleus (upper limbs, upper trunk). A non-dissociated upgaze palsy was present, with permanent downward deviation of the eyes. In the midbrain, the infarct was strictly unilateral and involved the riMLF iC, nD, PC, as well as the red nucleus, zona incerta, tegmental H field and fasciculus retroflexus tract. Classically, bilateral lesions in the *:; A ;t>*' <.2 Fig 3 (A) Transverse section through level of oculomotor nuclear complex (NU III) (approximately corresponding to that offig 2F). Asterisk points to right posterior thalamno-subthalamic paramedian artery. Note that on the left side the riMLF is entirely destroyed. (PAS stain; x 2). (B) Section parallel to that shown in (A). riMLF and nD can be recognised because of their relatively high content of myelinatedfibres. (Loyez stain; x 2). Bogousslavsky, Miklossy, Deruaz, Regli, Assal proven unilateral infarct of the upper midbrain are palsy.'o 13 16 - 18 However, upgaze palsy, which was summarised in table 2. The iC and nD were involved initially described by Henoch'9 and Parinaud,20 has in the four reported cases and in our case. In the first been associated with a presumed2'1- 23 or three cases, the riMLF was not described, but it approven2 8 50 13 24-26 unilateral mesencephalic lesion pears from the pathologic studies that it was very in a few cases. The cases of upgaze palsy with a probably damaged; it was involved in another case13 Table 2 Cases with upgaze palsyfrom a proven unilateral midbrain infarct 690 upper midbrain have been reported in vertical gaze Lesion (midbrain) * Freund, 1913 (2) Balthasar and Hopf, 1966 (28) Hatcher and Klintworth, 1966 (8) Christoff, 1974 (10) Pierrot-Deseilligny et al, 1982 (13)/Serdaru et al, 1982 (27) Present case downward deviation nD, iC, FR sparing of PC? nD, iC, degeneration of PC "from the superior colliculus into the pretectum post the PC and caused demyelination to it" intermittent nD, iC, FR, upper MLF demyelination of PC sustained nD, iC, FR, riMLF, PC Vertical oculocephalic manoeuvre preserved vertical deviations no deviation preserved vertical deviations no response from downward deviations nD: nucleus of Darkschewitsch, iC: nucleus interstitialis of Cajal, riMLF: rostral interstitial nucleus of the MLF, PC: posterior commissure, FR: fasciculus retroflexus. *In the 3 first cases the riMLF was not described. Table 3 Cases with proven left unilateral paramedian infarct of the thalamus Involvement of paramedian nuclei Involvement of other thalamic nuclei or connections Associated lesions Neuropsychological disturbances Freund, 1913 (2) Balthasar and Hopf, 1966 (28) pf, dm - somnolence Chiray et al, 1923 (3) "paramedian nuclei' dorsocaudal part Molnar, 1959 (6) 'paramedian nuclei' Tmth (with cm) midbrain (left), pyramidal tracts in the brainstem subthalamic area, cerebellar peduncle hippocampus, frontal cortex midbrain (left), scattered lesions in the right cerebral hemisphere midbrain (bilateral), cerebral hemispheres mesencephalic tegmentum and red nucleus (left) cerebral hemispheres midbrain (left), lenticular nuclei, cerebral hemispheres of the thalamus Gruner and Feuerstein, 1966 (7) cm Case B 'paramedian nuclei' Case S Sieben et al, 1977 (11) Case 2 Castaigne et al, 1981 (71) Case 9 'inferior part of the left thalamus', 'lacunes in the medial nuclei' vl, pu pf, dm, cm Case 19 pf, dm, cm Case 22 pf, dm, cm Case 26 Davous et al, 1984 (72) pf, dm, cm pf, dm, cm Present case pf, dm, cm anterior part of the ventrolateral region Tmth, pu anterior part of the ventrolateral region Tmth vIm, vlo vlm vp, (Tmth) (vlo) lacunae right anterior cerebral infarct not mentioned verbal perseverations, literal and verbal paraphasias, alexia, agraphia not mentioned 'sudden coma' not mentioned agitation, incoherence, confusion, disorientation in time and place unknown bilateral middle cerebral infarct, lacunae unknown midbrain (bilateral) brainstem and cerebellum (bilateral), left occipital lobe midbrain (left), scarce minute lesions in the cerebral hemispheres, ansa lenticularis, subthalamic nucleus somnolence, dysarthria reduced speech, initial somnolence, semantic paraphasias, perseverations initial somnolence and disorientation, anterograde amnesia, non-fluent and reduced speech, semantic (+ phonemic) paraphasias and parelexias, anomia, impairment of verbal memory, apathy pf = parafascicular nucleus, cm = centromedian nucleus, dm = dorsomedial nucleus, pu = pulvinar, Tmth = mamillo-thalamic tract (Vicq d'Azyr), vlo = ventral lateral nucleus-oral part, vlm = ventral lateral nucleus-medial part, vIc = ventral lateral nucleus--caudal part, vp = ventral posterior nucleus 691 Unilateral left paramedian infarction of thalamus and midbrain: a clinico-pathological study and in our patient. The PC was directly involved by al,13 where upgaze palsy was limited to smooth purthe infarct in one reported case10 and in our patient; suit movements, no downward deviation was present. Our patient showed aphasic disturbances with degenerated or demyelinated in two cases8 13 27; and appeared spared in one case.228 However, in the lat- reduction of speech, decreased verbal fluency, naming ter case, the efferent fibres that converge to the mid- difficulties, perseverations, semantic and less often line to form the PC were very probably involved as in phonemic paraphasias, semantic paralexias and disturbed spelling. Repetition was spared. Comprehencases with tumours apparently sparing the PC.29 The inputs involved in upgaze decussate in the sion was only slightly impaired. The unilateral left PC,13 1618 30 that a unilateral lesion involving the thalamic infarct involved the intralaminar, dorsoPC and its laterally spreading fibres can probably give medial, and ventral posterior nuclei of the thalamus, rise to an upgaze palsy, as in experiments in the mon- as well as the mamillo-tegmental tract, and a small key.31 However, no proven lesion limited to the PC portion of the posterior part of the ventral lateral nucleus. The cerebral hemispheres showed only scarce has ever been reported in man. The upgaze palsy did not spare the vestibular re- minute lesions in the central regions, which could not be responsible for the symptoms. The role of the thalsponse. Involvement of the PC does not abolish the vestibular-induced upward movements, because the amus in linguistic activities was initially discussed in vestibular inputs involved in upgaze do not follow the stimulation and electro-coagulation of the left thalPC and reach the oculomotor and trochlear nuclei, amus, with emphasis placed on the ventral lateral either directly from the vestibular nuclei, or indirectly nucleus and the pulvinar.41 43-46 Language disfrom a descending pathway probably originating in turbances have been reported in thalamic the iC.13 16 27 32. The absence of upward deviation on tumors46-48 and haemorrhages,49-58 with delinoculocephalic manoeuvre thus probably corre- eation of clinical syndromes suggesting motor, sensponded to involvement of the iC, as destruction of sory, or mixed transcortical aphasia. In thalamic the fibres of the PC do not alter vestibulo-ocular infarction, detailed aphasiological studies have been reflexes and because no lesion of the ascending made with CT correlations.59 67 Reduction of speech, anomia, perseverations and semantic vestibulo-oculomotor fibres was present. The eyes were permanently deviated downward. paraphasias were the most frequent alterations. Sustained or intermittent downgaze has been re- Involvement of the ventral lateral nucleus and pulported in diffuse encephalopathies33 and in intra- vinar has been usually suggested,45465962-646869 cranial hypertension.3435 Patients with a unilateral and could be related to connections with the prerolandic (ventral lateral nucleus) and postrolandic or bilateral thalamic haemorrhage may also show a downward deviation of the eyes,26 36 - 38 but they also (pulvinar) cortical speech areas.69 70 We have found 11 cases of infarction of the parashow intracranial hypertension. There is no report of sustained downgaze from a midbrain lesion without median part of the left thalamus with pathologic intracranial hypertension. In one case,13 27 an inter- confirmation in the literature (see table 3), either mittent downward deviation of the eyes was reported. without mesencephalic infarction, 3 71 or with It was proposed that this intermittent deviation could unilateral2 6 7 11 72 or bilateral7 71 midbrain have been due to transient firing of neurons in the involvement. Among these cases, neuropsychological riMLF and iC, from an interruption of ascending disturbances were mentioned only in three, being vestibulo-mesencephalic39 or descending cortico- either a confusional state,71 or aphasic symptoms mesencephalic inhibiting pathways. In our case, no very similar to those showed by our patient.6 72 significant lesion of the ascending vestibulo- Involvement of the ventral lateral and dorsomedial oculomotor pathways was present. The riMLF and nucleus with sparing of the pulvinar was present in iC were involved, and these structures are thought to one of the cases with speech disturbances,72 and no be major supranuclear centres involved in tonic verti- detailed topographical analysis was provided in the cal vestibular reflexes.16 18 Especially, the iC seems to other.6 Our case suggests that destruction of the pulhave some importance in the vertical semicircular ca- vinar and ventral lateral nucleus may not be necesnal vestibulo-ocular reflex and upward vestibulo- sary. Among the nuclei of the medial and intraocular movements.'0 Involvement of this nucleus laminar formations, the dorsomedial nucleus might be incriminated, because of connections with Broca's may have caused an imbalance in vestibulooculomotor regulation at the origin of the sustained area, Wernicke's area, and the gyrus supradownward deviation of gaze. Involvement of cortico- marginalis.69 Disturbances of verbal memory have mesencephalic fibres, with imbalance in the tonic in- also been attributed to involvement of the left dorputs that regulate vertical smooth pursuit42 seems somedial nucleus.65 7375 Although an extensive assessment of memory was more improbable. The localisation of these fibres is not known, and in the case 4 of Pierrot-Deseilligny et not realised, the findings in our patient suggested a so 692 Bogousslavsky, Miklossy, Deruaz, Regli, Assal marked anterograde amnesia, with inability to recall References any recent event. Older events were better recalled. Claude H, Loyez Mlle. Ramollissement du noyau rouge. There were no confabulations. Amnesic syndromes Rev Neurol (Paris) 1912;23:40-51. from thalamic infarcts have initially been studied in 2Freund SC. Zur Klinik und Anatomie der vertikalen cases with bilateral lesions,76 -78 most often in the Blicklahmung. Centralbl 1913;32: 1215-29. context of "thalamic dementia".'2 65 77 78 In necrop- 3Chiray M, Foix C,Neurol Nicolesco J. Henitremblement du type sied cases, involvement of the dorsomedial nuclei or de la sclerose en plaques par lesion rubro-thalamoof the mamillo-thalamic tract of Vicq d-Azyr has been sousthalamique. Syndrome de la region supero-externe emphasised,7' 78 but to our knowledge, there is no du noyau rouge avec atteinte silencieuse ou non du thalreport of a case with a unilateral thalamic infarct and amus. Ann Med (Paris) 1923;14:173-91. amnesia, which was pathologically studied. In cases 4Sigwald J, Monnier M. Syndrome thalamohypothalamique avec hemitremblement (ramwith CT study, involvement of the dorsomedial ollissement du territoire arteriel thalamo-perfore). Rev nucleus,65 73 75 ventral lateral nucleus, 65 73 75 or of Neurol (Paris) 1936;66:616-31. the anterior formation and mamillo-thalamic tract65 Schuster P. Beitrige zur Pathologie des Thalamus opticus has been suggested. In the 11 cases with a proven left I. Arch Nervenkrank 1936;105:358-432. paramedian infarction of the thalamus (see table 3), 6 Molnar L. Psychiat Die lokaldiagnostische Bedeutung der Vertithe memory was not studied. In our case, in the kalen Blicklfhmung; Beitriige zur Symptomatologie absence of lesion of the mamillo-thalamic tract and of und Faseranatomie des meso-diencephalen Obergangsthe anterior formation the amnesic disturbances were gebietes. Arch Psychiat Nervenkrank 1959;198:523-34. probably caused by severe lesion of the dorsomedial 7Gruner JE, Feuerstein J. Troubles de la conscience et tronc cerebral. Correlations anatomo-cliniques. In: Clinical nucleus. experiences in brain stem disorders (Inhasz IL ed.) Acta Marked underutilisation of the right side of the 25 Conventus Neuropsychiatricus et EEG Hungarici, body, with no spontaneous movement, abnormal Vallalat, Budapest 1966, 293-6. placement of the upper limb, poor withdrawal to Hatcher MA, Klintworth GK. The sylvian acqueduct pain, and motor impersistence were present, sugsyndrome. Arch Neurol 1966;15:215-22. gesting motor hemineglect.79 Motor neglect from a 9Jakimowicz K, Stefanko S, Pajak B. Ramollissements du thalamic lesion has been attributed to involvement of thalamus dans le territoire des pedicules arteriels venant de la cerebrale posterieure. Acda Med Pol 1968;9: the ventral lateral nucleus,80 81 of the centromedian 447-54. and parafascicular nuclei,82 or of the posterior part of the thalamus and pulvinar.83 No pathologic °Christoff N. A clinicopathologic study of vertical eye movements. Arch Neurol 1974;31:1-8. confirmation was provided in the latter two reports. G, de Reuck J, Van der Eecken H. Thrombosis of A case with a right thalamic haemorrhage was nec- "Sieben the mesencephalic artery. A clinico-pathological study ropsied,84 but detailed anatomical data were not of two cases and its correlation with the arterial vascuprovided. Our case may favour the theory of Watson larisation. Acta Neurol Belg 1977;77:151-62. et al,82 because the centromedian and parafascicular 12Castaigne P, Buge A, Cambier J, Escourolle R, Brunet P, nuclei were destroyed, whereas the ventral lateral Degos JD. Demence thalamique d'origine vasculaire nucleus showed only minor changes and the pulvinar par ramollissement bilateral limite au territoire du pedicule retro-mamillaire (i propos de 2 observations was spared. The motor neglect may have been due to anatomo-cliniques). Rev Neurol (Paris) 1966;114: global dysfunction of hemispheric activation, related 89-108. to involvement of these nuclei and of inputs from the C, Chain F, Gray F, Serdaru M, mesencephalic reticular formation.82 Except in one 3Pierrot-Deseilligny Escourolle R, Lhermitte F: Parinaud's syndrome. report,80 all series showed that thalamic neglect is Electro-oculographic and anatomical analyses of six more frequently caused by right than by left-sided vascular cases with deductions about vertical gaze lesions. However, our case shows that involvement of organization in the premotor structures. Brain the left intralaminar formation may cause motor 1982;105:667-96. neglect on the right side of the body. Involvement of 14 Eager RP. Selective staining of degenerating axons in the the mesencephalic reticular formation has also been central nervous system by a simplified method: spinal cord projections to external cuneate and inferior olivary suggested in some forms of unilateral neglect.85 Hownuclei in the cat. Brain Res 1970;22:137-41. ever, in our case, the unimodal aspect of the neglect suggests that the lesion of the upper mesencephalic '5Grafe MR, Leonard CM. Successful silver impregnation of degenerating axons after long survivals in the human reticular formation was not responsible. brain. J Neuropathol Exp Neurol 1980;39:555-74. 16Bender MB. Brain control of conjugate horizontal and The authors thank H Van der Loos, MD, University Department of Anatomy, Lausanne, for his helpful comments. vertical eye movements. A survey of the structural and functional correlates. Brain 1980;103:23-69. 17 Trojanowski JQ, Lafontaine MH. Neuroanatomical correlates of selective downgaze paralysis. J Neurol Sci 198 1;52:91-101. 18 Buttner-Ennever JA, Buttner U, Cohen B, Baumgartner Unilateral left paramedian infarction of thalamus and midbrain: a clinico-pathological study G: Vertical gaze paralysis and the rostral interstitial nucleus of the medial longitudinal fasciculus. Brain 1982;105:125-49. 9Henoch EH. Tuberkulose der Corpora quadrigemina. Berlin Klin Wochschr 1984;1:125-7. 20Parinaud H. Paralysie des mouvements associes des yeux. Arch Neurol 1883;5:145-72. 21 Nashold BS Jr, Seaber JH. Defects of ocular motility after stereotactic midbrain lesions in man. Arch Ophthalmol 1972;88:245-8. 22Seaber JH, Nashold BS Jr: Comparison of ocular motor effects of unilateral stereotactic midbrain lesions in man. Neuro-ophthalmol 1980;1:95-8. 23Smith MS, Laguna JF. Upward gaze paralysis following unilateral pretectal infarction. Arch Neurol 1981; 38:127-9. 24Reich F. Herd im Thalamus opticus. Neurol Centralbi 1904;14:662. Van Gehuchten P. Syndrome de Parinaud. Etude anatomique. J Beige Neurol Psychiat 1940;40:126-33. 26K6rnyey A: Blickstorungen bei vascularen Herden des meso-diencephalen Obergangsgebietes. Arch Psychiat Nervenkrank 1959;198:535-43. 27Serdaru M, Gray F, Lyon-Caen 0, Escourolle R, Lhermitte F. Syndrome de Parinaud et deviation tonique verticale du regard. Trois observations anatomocliniques. Rev Neurol (Paris) 1982;138:601-17. 28Balthasar K, Hopf A: Die Freund-Vogt'sche Herdbildung bei supranuklearer Heberlihmung der Augen mit Lidretraktion. Dtsche Zt Nervenheilk 1966;189:275-96. 29 Moffie D, Ongerboer de Visser BW, Stefanko SZ. Parinaud's syndrome. J Neurol Sci 1983;58:175-83. 30 Bogousslavsky J, Regli F. Upgaze palsy and monocular paresis of downward gaze from ipsilateral thalamomesencephalic infarction: A vertical "one-and-a-half" syndrome. J Neurol 1984;231:43-45. 31 Pasik P, Pasik T, Bender MB. The pretectal syndrome in monkeys. I. Disturbances of gaze and body posture. Brain 1969;92:521-34. 32Pola J, Robinson DA. Oculomotor signals in medial longitudinal fasciculus of the monkey. J Neurophysiol 1978;41:245-59. 33Keane JR, Rawlinson DG, Lu AT. Sustained downward deviation. Two cases without structural pretectal lesions. Neurology (Minneap) 1976;26:594-5. 34Lundberg N: Continuous recording and control of ventricular fluid pressure in neurosurgical practice. Acta Psychiatr Neurol Scand 1960;36 (suppl): 1-193. Hoyt W, Daroff RB. Supranuclear disorders of ocular control systems in man. In: The control of eye movements (Bach y Rita P, Collins CC, Hyde JE, eds), New York, Academic Press 1971:175-235. 36Fisher CM. Some neuro-ophthalmologic observations. J Neurol Neurosurg Psychiatry 1967;30:383-92. 37Lapresle J, Said G. Deviation forcee des yeux vers le bas et en dedans et mouvements oculaires periodiques au cours d'une hemorragie anevrysmale de la calotte mesencephalique. Rev Neurol (Paris) 1977;133:497-503. 38Gilner LI, Avin B. A reversible ocular manifestation of thalamic hemorrhage. A case report. Arch Neurol 1977;34:715-6. 39Tarlov E. Anatomy of the two vestibulo-oculomotor 693 projection systems. In: Brodal A, Pompeiano 0, eds. Basic aspects of central vestibular mechanisms Amsterdam, Elsevier 1972:471-91. 40Anderson JH. Behavior of the vertical canal VOR in normal and INC-lesioned cats. In: Fuchs AF, Becker W, eds. Progress in Oculomotor Research Amsterdam, Elsevier 1981:396-401. 41Guiot G, Hertzog E, Rondot P, Molina P. Arrest or acceleration of speech evoked by thalamic stimulation in the course of stereotaxic procedures for parkinsonism. Brain 1961;84:363-9. 42Barontini F, Simonetti C, Ferranini F, Sita D. Persistent upward eye deviation. Report of two cases. Neuroophthalmol 1983;3:217-24. 43Krayenbiihl H, Siegfried J, Kohenof M, Yasargil MG. Is there a dominant thalamus? Confin Neurol 1965; 26:246-9. "4Bell DS. Speech function of the thalamus inferred from the effects of thalamotomy. Brain 1968;91:619-38. 45Ojemann GA, Fedeo P, Van Buren JM. Anomia from pulvinar and subcortical parietal stimulation. Brain 1968;91:99-117. 46Ojemann GA, Ward AA. Speech representation in the ventro-lateral thalamus. Brain 1971;91:99-117. 47Smythe GE, Stern K. Tumors of the thalamus. A clinicopathological study. Brain 1938;61:339-74. 48McKissock W, Paine KWE. Primary tumors of the thalamus. Brain 1958;81:41-63. 49Cheek WR, Taveras J: Thalamic tumors. J Neurosurgery 1966;24:505-13. 50Bugiani 0, Conforto C, Sacco G. Aphasia in thalamic hemorrhage. Lancet 1969;i:1052. s1Ciemens VA. Localized thalamic hemorrhage. A cause of aphasia. Neurology (Minneap) 1980;20:776-82. 52Mohr JP, Watters WC, Ducan GW. Thalamic hemorrhage and aphasia. Brain Lang 1975;2:3-17. SLuria AR. A quasi-aphasic speech disturbance in lesions of the deep structures of the brain. Brain Lang 1977; 4:432-59. 54Reynolds AF, Turner PT, Harris AB, Ojemann GA, Davis LE. Left thalamic hemorrhage with dysphasia. Brain Lang 1979;7:62-73. sCappa SF, Vignolo LA. "Transcortical" features of aphasia following left thalamic hemorrhage. Cortex 1979;15:121-30. S6Alexander MP, Lo Verme SR Jr. Aphasia after left hemispheric intracerebral hemorrhage. Neurology (Minneap) 1980;30:1193-202. S7Assal G, Lanares J. Syndrome amnesique transitoire lors d'un hematome thalamique gauche. Congres de psychiatrie et de neurologie, Barcelone 1982:265-70. S8Papagno C, Guidotti M. A case of aphasia following left thalamic hemorrhage. Eur Neurol 1983;22:93-95. SElghozi D, Strube E, Signoret JL, Cambier J, Lhermitte F. Quasi-aphasie lors de lesions du thalamus. Relation du trouble du langage et de l'activation elective de l'hemisphere gauche dans 4 observations de lesions thalamiques gauches et droites. Rev Neurol (Paris) 1978;134:557-74. 60 Mazaux JM, Orgogozo JM, Henry P, Loiseau P. Troubles du langage au cours des lesions thalamiques. Etude par le test de Goodglass et Kaplan. Rev Neurol (Paris) 694 1979;135:59-64. 61 Demeurisse G, Derouck M, Coekaerts MJ, et al. Study of two cases of aphasia by infarction of the left thalamus. Acta Neurol Belg 1979;79:450-9. 62Cohen JA, Gelfer CE, Sweet RD. Thalamic infarction producing aphasia. Mt Sinai J Med (NY) 1980; 47:398-404. 63Archer CR, Ilinsky IA, Goldfader PR, Smith KR Jr. Aphasia in thalamic stroke: CT stereotactic localization. J Comp Assist Tomogr 198 1;5:427-32. 64McFarling D, Rothi LJ, Heilman KM. Transcortical aphasia ischaemic infarcts of the thalamus: a report of two cases. J Neurol Neurosurg Psychiatry 1982; 45:107-12. 65 Michel D, Laurent B, Foyatier N, Blanc A, Portafaix M. Infarctus thalamique paramedian gauche. Etude de la memoire et du langage. Rev Neurol (Paris) 1982; 138:533-50. 66Graff-Radford NR, Eslinger PJ, Damasio AR, Yamada T. Non-hemorrhagic infarction of the thalamus. Behavioral, anatomic and physiologic correlates. Neurology (Cleveland) 1984;34:14-23. 67Gorelick PB, Hier DB, Benevento L, Levitt S. Aphasia after left thalamic infarction. Arch Neurol 1984; 41:1296-8. 68 Ojemann GA. Subcortical language mechanisms. In: Neurolinguistics Whitaker H, Whitaker HA, eds. Vol 1, New York Academic Press, 1976:103-38. 69 Van Buren JM, Borke RC. Alterations in speech and the pulvinar. Brain 1979;92:255-84. 70Roch Lecours A, Lhermitte F. L'aphasie. Paris Flammarion, 1979:193-222. 71 Castaigne P, Lhermitte F, Buge A, Escourolle R, Hauw JJ, Lyon-Caen 0. Paramedian thalamic and midbrain infarcts: clinical and neuropathological study. Ann Neurol 1981;10:127-48. 72Davous P, Bianco C, Duval-Lota AM, De Recondo J, Vedrenne C, Rondot P. Aphasie par infarctus thalamopedonculaire gauche. Observation anatomo-clinique. Rev Neurol (Paris) 1984;140:711-9. Bogousslavsky, Miklossy, Deruaz, Regli, Assal 73Squire LR, Moore RY: Dorsal thalamic lesion in a noted case of human memory dysfunction. Ann Neurol 1979;6:503-6. 74 Speedie LJ, Heilman KM. Anterograde memory deficits for visuospatial material after infarction of the right thalamus. Arch Neurol 1983;40: 183-6. 75Goldenberg G, Wimmer A, Maly J. Amnesic syndrome with a unilateral thalamic lesion: a case report. J Neurol 1983;229:79-86. 76 Schott B, Mauguiere F, Laurent B, Serclerat 0, Fischer C. L'amnesie thalamique. Rev Neurol (Paris) 1980; 136:117-30. 77Guberman A, Stuss D. The syndrome of bilateral paramedian thalamic infarction. Neurology (NY) 1983; 33:540-6. 78 Poirier J, Barbizet J, Gaston A, Meyrignac C. Demence thalamique. Lacunes expansives du territoire thalamomesencephalique paramedian. Hydrocephalie par st6nose de l'acqueduc de sylvius. Rev Neurol (Paris) 1983;139:349-58. '9 Laplane D, Degos JD. Motor neglect. J Neurol Neurosurg Psychiatry 1983;46: 152-8. 80Zoll JG. Transient anosognosia associated with thalamotomy: is it caused by proprioceptive loss? Confin Neurol 1969;31:48-55. 81 Laplane D, Escourolle R, Degos JD, Sauron B, Massiou H. La negligence motrice d'origine thalamique. A propos de deux cas. Rev Neurol (Paris) 1982;138:201-1 1. 82 Watson RT, Valenstein EV, Heilman KM. Thalamic neglect. Possible role of the medial thalamus and nucleus reticularis in behaviour. Arch Neurol 198 1;38:501-6. 83Schott B, Laurent B, Mauguiere F, Chazot G. Negligence motrice par hematome thalamique droit. Rev Neurol (Paris) 1981 ;137:447-55. "Watson RT, Heilman KM. Thalamic neglect. Neurology (Minneap) 1979;29:690-4. 85 Watson RT, Heilman KM, Miller BD, King FA. Neglect after mesencephalic reticular formation lesions. Neurology (Minneap) 1974;24:294-8.