Lateral Thalamic Infarcts Louis R. Caplan, MD; L. Dana DeWitt, MD; Michael S. Pessin, MD; Phillip B. Gorelick, MD; Lester S. Adelman, MD \s=b\ A patient with occlusion of the proximal posterior cerebral artery (PCA), a lateral thalamic infarct, and hemisensory loss later developed hemianopia and hemiparesis and had extensive PCA territory infarction in the midbrain, the lateral portion of the thalamus, and the occipital lobe noted at necropsy. Two other patients had lateral thalamic infarcts on computed tomography, normal angiographic findings, and presumed thalamogeniculate artery branch occlusion. There are three clinical syndromes associated with lateral thalamic infarction: (1) hemisensory loss, hemiataxia, and involuntary movements; (2) pure sensory stroke; and (3) sensory-motor stroke. Ataxia, adventitious movements, and sensory loss are due to infarction of the lateral, posterolateral, and posteromedial ventral nuclei caused by occlusion of the PCA proximal to the thalamogeniculate artery branches or by occlusion of large thalamogeniculate arteries. Pure sensory and sensory\x=req-\ motor strokes are due to smaller infarcts in the posterolateral-posteromedial ventral complex and adjacent internal capsule caused by occlusion of penetrating artery branches of the thalamogeniculate arteries. (Arch Neurol 1988;45:959-964) puted tomography (CT) and magnetic resonance imaging now accurately define these deep hemispheral in¬ farcts. Within the anterior circula¬ tion, angiography and necropsy showed two patterns of vascular occlusion in patients with infarcts in the internal capsule, pallidum, and striatum: (1) occlusion of penetrating lenticulostriate46 or anterior choroidal artery7 branches and (2) obstruc¬ tion of the parent supraclinoid inter¬ nal carotid8 or main-stem middle cere¬ bral arteries1'8-9 before the origin of the penetrating arteries. The posterior circulation lesion that is analogous to deep hemispheral is¬ chemia is lateral thalamic infarction. The clinical features were described in the beginning of the 20th century.1014 The anatomy of thalamic blood supply has been clarified by injection and microangiography techniques,1520 and CT can define the distribution of tha¬ lamic infarcts,2124 but the vascular pathology causing lateral thalamic infarcts has rarely been studied. We now report clinical, CT, angiographie, and necropsy data obtained from patients with lateral thalamic in¬ farcts to clarify the clinical features and vascular causes. REPORT OF CASES Tnfarcts in the basal ganglia and cerebral white matter cause clini¬ cal syndromes that differ from corti¬ cal infarcts of comparable size.13 Com- Accepted for publication Jan 25, 1988. From the Departments of Neurology (Drs Caplan, DeWitt, and Pessin) and Neuropathology (Dr Adelman), New England Medical Center, Tufts University, Boston, and the Departments of Neurology, Michael Reese Hospital, Chicago, and the University of Chicago (Dr Gorelick). Reprint requests to Department of Neurology, New England Medical Center, Tufts University, 171 Harrison Ave, Boston, MA 02111 (Dr Caplan). Case 1.—A 69-year-old white man awak¬ ened with dizziness; shortly thereafter, he required support to walk. He had dietcontrolled diabetes mellitus, hypertension, surgical repair of a traumatic tear of the aorta, and a surgical bypass for occlusive disease of the right leg. Examination showed severe sensory loss of all modali¬ ties including pin, temperature, touch, position sense, and vibration in the left side of the face and trunk and the left limbs. The right pupil was smaller (2 mm vs 3 mm on the left) and reacted poorly to light. There was slight weakness in the left side of the face only. The left plantar Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 05/29/2015 equivocal; deep tendon symmetrical. The initial findings of CT were normal. Two days response reflexes was were later, CT showed an area of low attenua¬ tion in the right lateral portion of the thalamus. Three days after admission, the patient's eyes became conjugately deviated to the right at rest, but moved conjugately to the left to follow visual objects. There was a left homonymous hemianopia. The patient read only the right side of the printed page. The left hemisensory loss was unchanged, and there was no change in weakness. Repeated CT showed the pre¬ viously described right thalamic infarct, with new areas of low attenuation in the medial part of the temporo-occipital lobes as well as in the lateral geniculate nucleus, compatible with new infarcts (Fig 1). Heparin therapy was begun. Angiography showed occlusion of the perimesencephalic portion of the right posterior cerebral artery (PCA). There was also subcriticai stenosis of the distal left vertebral and basilar arteries. There was suboptimal visualization of the left PCA possibly sec¬ ondary to stenosis of the P-l segment. The right PCA did not originate from the right internal carotid artery, but collateral ves¬ sels from the right middle cerebral artery filled the right PCA in a retrograde direc¬ tion. Cardiac studies revealed a recent myo¬ cardial infarct and frequent premature ventricular contractions. On the 23rd hos¬ pital day, the patient had a massive gastro¬ intestinal hemorrhage. Laparotomy re¬ vealed severe erosive gastritis, and a gastrectomy was performed. Postoperatively, the myocardial infarct was extended, and the patient had pulmonary edema, pneu¬ monia, and intermittent hypotension. A month after admission, he developed a complete left hemiplegia. His hemianopia and hemisensory loss were unchanged. He had renal failure and hypotension, and died six weeks after his initial stroke. Necropsy revealed occlusion of the prox¬ imal 2 cm of the right PCA by a graybrown granular thrombus. There was an atherosclerotic plaque at the origin of the artery that had severely narrowed the lumen. There was a 1 X 2 X 3-cm irregular Fig 1.—Case 1, Computed tomographic scan shows infarct in lateral portion of thalamus (single arrow) and occipital lobe posterior to lateral ventricle (double arrow). softening in the right lateral por¬ tion of the thalamus, extending from the level of the massa intermedia to the splenium of the corpus callosum (Fig 2). The right cerebral peduncle and substantia nigra were also recently softened (Fig 3), and there was a recent infarct in the right medial portion of the occipital lobe. Histologically, the thalamic softening was com¬ posed of several confluent infarcts, some of which were subacute and others that were recent. A microscopic old infarct was present in the left side of the thalamus. Case 2.—A 64-year-old white man noted numb, tingly feelings in his left arm while driving a car. The numbness spread to his left cheek and leg, and walking was clum¬ sy. The patient had experienced two prior transient spells of numbness, tingling, and clumsiness of the left arm two and three months before, respectively. He had a his¬ tory of diabetes mellitus, hypertension, and two myocardial infarcts. Examination showed slight weakness in the left side of the face and slight clumsiness and ataxia in the left arm and leg. Sensitivity to pin and light touch was reduced on the left. The patient's gait was slightly unsteady. His reflexes were symmetrical, and his plantar reflexes were flexor. Computed tomography showed a small right lateral thalamic infarct. Angiographie findings were normal except for a slight nonstenosing plaque in the distal extracranial por¬ tion of the right vertebral artery. The right PCA and its branches were normal. The patient's left-sided clumsiness gradually improved, but subjective sensory symp¬ toms remained in the left limbs. Case 3.—A 60-year-old Chinese man noted prickling paresthesia of his left arm, hand, and leg. Later, these spread to include the left side of his face, the inside of his mouth, and his left thumb. His left arm and leg were slightly uncoordinated. He had no important past illnesses. On examination there was slight subjective decrease in pin and touch sensation in the left limbs. Position sense was less accurate in the left hand and foot. There was slight ataxia and uncoordination of the left limbs on finger-to-nose testing, and the patient's zone of Fig 2.—Case 1, Thalamic infarct (arrow) at necropsy. Right hemisphere on right side of illustration. Fig 3.—Case 1, Right cerebral peduncle and substantia nigra are soft and necrotic. These structures are on left side of illustration. gait was slightly ataxic. Strength, reflexes, and plantar responses were normal. He had slight dysarthria. His blood pressure was elevated throughout his hospitalization, and he had glycosuria and an elevated serum glucose level that ranged from 12.1 to 21.3 mmol/L. Computed tomography showed a small lacune in the right putamen and an infarct in the right ventrolateral portion of the thalamus (Fig 4). Angiography showed a normal right PCA and no important stenosis of intracranial or extracranial arteries. The patient was treated with antihypertensive and oral antihyperglycemic agents. Walking gradu¬ ally improved. He was readmitted to the hospital for left-sided pure motor hemiplegia, and CT showed no new lesions. Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 05/29/2015 COMMENT We have described two different vascular lesions in patients with lat¬ eral thalamic infarcts. In one patient, occlusion of the PCA proximal to the thalamogeniculate artery branches caused a large lateral thalamic infarct that was later complicated by pro¬ gressive symptoms and ischemia in the cerebral peduncle and occipital lobe. Two other patients, each with hypertension and diabetes, had more restricted lateral thalamic infarcts and normal opacification of the PCA. These infarcts were gradually pro¬ gressive or preceded by transient is- Fig 4.—Case 3, Computed tomographic scan shows hypodensity in right portion of lateral thalamus (arrow). chemic attacks, and there were no recognized proximal sources of embo¬ li. The background diathesis for small-vessel disease, absence of docu¬ mented large-vessel occlusive disease, and lack of a known source for emboli make it very probable that the patients had intrinsic occlusive dis¬ ease of the thalamogeniculate arter¬ ies, but necropsy verification was not available. These vascular lesions and their resultant infarcts are diagramed in Fig 5 and are compared with the arterial lesions causing striatocapsular infarction. A review of the rele¬ vant vascular and brain anatomy, his¬ torical observations, clinical findings, and imaging abnormalities explains the various syndromes and their vas¬ cular causes in patients with lateral thalamic infarction. Relevant Vascular and Brain Anatomy The "thalamogeniculate pedicle" of arteries arises from the ambient seg¬ ment of the PCA and penetrates into the thalamus between the geniculate bodies. The pedicle consists of six to ten arteries that vary widely in diam¬ eter and originate together. These vessels are the posterior circulation counterpart of the lenticulostriate middle cerebral artery branches that supply the striatum and internal cap¬ sule. All levels of the brain stem are irrigated by midline large, penetrat¬ ing, and long and short circumferen¬ tial arteries. The thalamogeniculate pedicles have short circumferential branches that supply the ventrolateral portion of the thalamus including the posterolateral and posteromedial ventral nuclei, the inferior and poste¬ rior portions of the ventralis lateralis, the lateral portion of the centróme- Fig 5.—Diagram illustrating mechanisms of deep infarction. Top left, Basal ganglionic capsular infarction due to middle cerebral artery occlusion (arrow). Top right, Smaller deep capsular infarct due to lenticulostriate artery occlusion (arrow). Bottom left, Lateral thalamic infarct due to posterior cerebral artery occlusion (arrow). Bottom right, Lateral thalamic infarct due to thalamogeniculate artery occlusion (arrow). nucleus, and the rostrolateral portion of the pulvinar. The polar and thalamoperforating arteries are middian line penetrators, and the cortical branches of the PCA are analogous to the large circumferential arteries. The posterolateral choroidal arteries arise from the PCA, just distal to the thalamogeniculate arteries. Historical Observations Dejerine and Roussy11 described and explained the findings in patients with infarcts in the ventroposterolateral portion of the thalamus, which they designated le syndrome thalamique. Clinical findings came from two cases reported previously by Dejerine and Egger10 and from three reported by their colleagues Dide and Durocher12 and Chinny.14 The microscopic pathologic findings of three of these cases were reviewed for the first time (Fig 6, top left, center, and right).11 All signs were contralateral to the tha¬ lamic infarct and included (1) a rapid¬ ly regressing slight hemiparesis; (2) a more prominent and persistent senso¬ ry abnormality affecting both "super¬ ficial" (touch, pin, and temperature) and "deep" (articular and propriocep- Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 05/29/2015 tive) modalities (The patients also showed delayed and distorted percep¬ tion, inability to localize sensation, and astereognosis. Sensory abnormal¬ ities affected the face, limbs, and trunk.); (3) hemiataxia (The contralateral limbs were hypotonie and uncoordinated, a finding the authors related to the sensory loss.); (4) abnor¬ mal spontaneous movements (hemi- chorea and hemiathetosis with spon¬ taneous movements, usually small, of the hand and digits, occasionally with an undulating, rhythmic character at times resembling tremor [hemitremblementj); and (5) pain and dysesthesia that developed later on the hemianesthetic side. Deep tendon reflexes were normal or only slightly exagger¬ ated, and there was no Babinski's sign. Facial weakness was common. Some patients had dysphagia, sphinc¬ ter abnormalities, and "vasomotor" abnormalities such as a cyanotic, cool hand on the affected side. Dejerine and Roussy11 did not comment on the location or nature of the vascular lesion. Foix and Hillemand13 reviewed the anatomy and vascular supply of the thalamus and elaborated on what mand13 used to illustrate this point. Necropsy studies have since docu¬ mented the frequent coexistence of lateral thalamic and cortical PCA ter¬ ritory infarcts.2731 Figure 7 shows a restricted infarct localized to thala¬ mogeniculate territory at necropsy. Vascular Etiology and Symptoms of PCA Occlusion When the location and cause of occlusive lesions within the posterior circulation were analyzed at necropsy, Castaigne et al28 noted that most occlusions of the PCA affected corti¬ cal branches and were caused by cardiogenic or intra-arterial embolism. An angiographie study of 23 patients who had both hemianopia and occipi¬ tal infarction seen on CT showed a high incidence of embolism to the PCA or its branches,32 and PCA embo¬ lism was common in the Michael Reese Stroke Registry.33 In situ steno¬ sis and occlusion of the PCA are more common in blacks than in whites.34 Atherostenosis of the PCA most often affects the proximal segments of the artery.35 Fig 6.—Top left, center, and right, Drawings represent three cases. Anatomy was not marked. Ependymal lining of third ventricle is on left and insular cortex on right. Black represents infarcts all cutting across posterior limb of internal capsule (from Dejerine and Roussy"). Bottom, Drawing Illustrates frequent coexistence of lateral thalamic and temporo-occipital lobe infarction (in black) (from Foix and Hillemand13). Fig 7.—Typical restricted lateral thalamic infarct at necropsy (arrowhead). they called the syndrome of the thal¬ amogeniculate pedicle. In addition to the signs noted by Dejerine and Roussy,11 they added a description of the "thalamic hand," which is flexed and pronated, with the thumb trapped within the other digits. Sensory symp¬ toms could be limited to the face, an arm, or a leg and could even mimic a radicular distribution.16-25 Cerebellar signs were caused by interruption of the thalamic termination of superior cerebellar peduncle fibers originating in the cerebellum. Foix and Hillemand13 and Foix and Masson26 noted the frequent association of the tha¬ lamic syndrome with a hemianopia, dubbing this combination the syn¬ drome of the PCA. Figure 6, bottom, is a copy of the diagram Foix and Hille- Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 05/29/2015 The most frequent symptoms of PCA occlusive disease are caused by infarction within the temporo-occipital lobes and include visual field, read¬ ing, and memory abnormalities.30·36-37 Early authors noted signs of dysfunc¬ tion of the rostral portion of the midbrain and thalamus in the territories of the thalamoperforating and thalmogeniculate arteries due to PCA occlusion.13-26 Benson and Tomlinson38 reported hemiplegia caused by proxi¬ mal PCA occlusion affecting the cere¬ bral peduncle, a finding that devel¬ oped later in the course of our patient 1. Another patient had occlusion of the PCA just before the ambient seg¬ ment on angiography and had contralateral paresis and sensory loss with¬ out hemianopia.3' Fisher40 briefly described three patients with severe stenosis of the proximal PCA among a large group of patients with transient spells of unilateral numbness; in one patient, the spells were followed by a major PCA territory infarct. Symp¬ toms of ischemia of the midbrain and thalamus occur only when the PCA is occluded proximally before the origin of the thalamoperforating, thalamo¬ geniculate, and choroidal artery branches. Brain Imaging Computed tomography and MRI accurately localize thalamic infarcts. In patients with PCA dis¬ can now ease, infarcts seen on CT scans are most often localized in the territories of cortical branches.32-41 In one re¬ ported case, a low-density CT lesion in the lateral portion of the thalamus in a patient with the thalamic syndrome probably represented an old, small hematoma.21 A study of CT localiza¬ tion of 25 thalamic infarcts described 11 patients with clinically diagnosed lateral thalamic infarcts, nine of whom had CT lesions in the thalamo¬ geniculate territory; six of whom had visual field defects; and four of whom had additional PCA territory cortical infarcts.23 Angiography, however, was not performed in every case. Takahashi et al24 analyzed the CT findings in 22 patients with thalamic infarcts. The thalamogeniculate territory was involved in nine of the patients, and all had severe stenosis or occlusion of the PCA, which was embolie in at least one patient. Thalamogeniculate artery lesions were limited to the posterolateral and posteromedial ven¬ tral nuclei, the lateral portion of the centromedian nucleus, and rostrolateral pulvinar. Two patients had CT lesions in the thalamogeniculate and cortical PCA territories, and four patients had lesions in the thalamoge¬ niculate, posterolateral choroidal, and cortical PCA territories. The postero¬ lateral choroidal artery arises adja¬ cent to the thalamogeniculate pedicle, and supplies the dorsolateral and pos¬ terior pulvinar territory adjacent to the thalamogeniculate supply. In one series of 38 patients with PCA occlu¬ sion seen on angiography, four patients had thalamogeniculate in¬ farcts on CT, and three of these four had additional cortical infarction.22 Among 50 PCA territory infarcts in another series, 15 were deep (thalam¬ ic), 24 were cortical, and 11 were mixed.36 While proximal posterior cerebral occlusion can cause infarc¬ tion limited to the thalamogeniculate territory, more often there are accom¬ panying lateral posterior choroidal and cortical infarcts. The clinical findings in the reported cases of CTdocumented thalamogeniculate terri¬ tory infarction were similar to those in our cases: slight transient hemi¬ paresis, hemiataxia with involuntary small hand movements, and a promi¬ nent hemisensory loss. One patient, similar to our patient 1, was a 67year-old woman with left hemihypesthesia and hemiataxia who reported dizziness, gait ataxia, and hallucina¬ tions.31 The thalamic infarct was large and included the thalamogeniculate territory, with some additional medial thalamic extension, and the causative vascular lesion was stenosis of the ambient portion of the right PCA. Prior Reports of Syndromes of Lacunar Infarcts in the Lateral Portion of the Thalamus Occlusion of small, deep, penetrat¬ ing artery branches is also a recog¬ nized cause of restricted lateral tha¬ lamic infarction. Fisher42·43 described serial section analyses in two patients with lacunar infarcts limited to the ventral posterior somatosensory nu¬ clei of the thalamus. The cause of the vascular lesion was severe lipohyalinosis with disorganization of the arte¬ rial wall and obstruction of the lum¬ in diame¬ ens of arteries 2 to 400 µ ter. The proximal PCA was normal. Clinical findings consisted of tran¬ sient spells or strokes in which the symptoms were limited to numbness, dysesthesia, and paresthesia, most often in the contralateral portion of the face, limbs, and trunk. Objective threshold sensory loss was usually slight.6·40·42·43 Necropsy performed in another patient with right hemipare¬ sis and hemisensory loss showed a lacune in the ventroposterior nuclei, with pallor of the adjacent internal capsule caused by penetrating artery disease.44 In two other necropsies, sensory motor stroke was associated with infarction of the ventroposterior por¬ tion of the thalamus and adjacent internal capsule.6 The original report of Dejerine and Roussy11 included drawings of three infarcts that caused the thalamic syndrome (Fig 6, top left, center, and right). All were larger than lacunes and involved the ventrolateral portion of the thalamus, and all had small tonguelike extensions into the posterior limb of the internal capsule and posterior putamen. The authors did not analyze the vascular lesion, and we could not find a report documenting the vascular pathology in a patient with a ventrolateral tha¬ lamic infarct of comparable size and location. Clinical Separation of Syndromes Several clinical clues help separate PCA disease from branch disease of the thalamogeniculate artery. These include (1) the lesions observed on CT are somewhat larger; (2) CT lesions are not restricted to thalamogenicu¬ late territory but may also include the pulvinar, the more medial portion of the thalamus, or portions of the infe¬ rior temporal or occipital lobes; and (3) the clinical syndrome may include elements not usually a part of the thalamic syndrome. Patient 1 showed neglect of the left side of space, conju¬ gate deviation of the eyes to the ipsi- Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 05/29/2015 lateral side, and hemianopia, findings that, to our knowledge, have not been described in thalamogeniculate terri¬ tory infarction. These signs developed only when infarction was noted on CT in the temporal and occipital lobes. We have seen one other patient with conjugate eye deviation in a combined thalamic-superficial PCA territory infarct; conjugate eye deviation does not usually accompany hemianopia in patients with restricted temporooccipital infarcts. Neglect has been described in unilateral rostral brainstem lesions, usually involving the medial midbrain tegmentum and the medial portion of the thalamus.7·45'48 Progression of signs, especially if it is stepwise and occurs during a peri¬ od of weeks, is unusual in branch dis¬ ease. The findings in thalamogeniculate branch occlusion infarction also differ from pure sensory stroke. Patients have abnormal motor signs of tran¬ sient hemiparesis and incoordination, tremor, and abnormal spontaneous movements ("chorea or tremor") on the side of the sensory loss. The motor abnormalities are probably caused by interruption of extrapyramidal path¬ ways from the ansa lenticularis and cerebellifugal fibers from the superior cerebellar peduncle and red nucleus that synapse in the ventrolateral nucleus of the thalamus and by involvement of the posterior limb of the internal capsule adjacent to the thalamus. We have also noted a slight but definite gait ataxia that is often more severe than the ataxia of the contralateral limbs. When infarction is limited to the posterior portion of the ventral nuclei (pure sensory stroke) patients report numbness and paresthesia, but there rarely is objec¬ tive decrease in somatosensory thresholds. These smaller infarcts are probably due to disease of smalldiameter thalamogeniculate artery branches. A slightly larger branch probably irrigates both the lateral portion of the thalamus and the poste¬ rior portion of the internal capsule and putamen; occlusion causes a sen¬ sory-motor stroke. When infarcts are larger and affect fibers passing from the medial and lateral portions of the thalamus to the cortical sensory zones, sensory loss is more severe and "thalamic pain" often develops later. Unfortunately, there have not been enough morphological studies per¬ formed that characterize the underly¬ ing vascular pathology within the thalamogeniculate pedicle. Normal angiographie findings and the fre¬ quency of coexistent lacunes, hyper- tension, and diabetes (risk factors for penetrating artery disease) suggest that the lesion is similar in most cases to other basilar branch infarcts.49·50 In some patients, occlusion of the PCA infarct limited to thal¬ amogeniculate territory. How many of these patients will progress, as our can cause an patient 1 did, to having a more exten¬ sive infarct in the PCA territory is unknown. References 1. Caplan LR, Babikian V, Helgason C, et al: Occlusive disease of the middle cerebral artery. Neurology 1985;35:975-982. 2. Damasio A, Damasio H, Rizzo M, et al: Aphasia with nonhemorrhagic lesions in the basal ganglia and internal capsule. Arch Neurol 1982;39:15-20. 3. Naeser MA, Alexander M, Helm-Estabrooks N, et al: Aphasia with predominantly subcortical lesion site. Arch Neurol 1982;39:2-14. 4. Fisher CM: Pure motor hemiplegia of vascular origin. Arch Neurol 1965;13:30-44. 5. Fisher CM: The arterial lesion underlying lacunes. Acta Neuropathol 1967;12:1-15. 6. Mohr JP: Lacunes, in Barnett HJ, Mohr J, Stein B, et al (eds): Stroke: Pathophysiology, Diagnosis, and Management. New York, Churchill Livingstone Inc, 1986, pp 475-486. 7. Helgason C, Caplan LR, Goodwin J, et al: Anterior choroidal artery territory infarction: Case reports and review. Arch Neurol 1986;3:681\x=req-\ 686. 8. Bladin P, Berkovic S: Striatocapsular infarction: Large infarcts in the lenticulostriate arterial territory. Neurology 1984;34:1423-1430. 9. Adams H, Damasio H, Putnam S, et al: Middle cerebral artery occlusion as a cause of isolated subcortical infarction. Stroke 1983; 14:948-952. 10. Dejerine J, Egger M: Contribution a l'etude de la physiologie pathologique de l'incoordination motrice. Rev Neurol 1903;11:397-405. 11. Dejerine J, Roussy G: Le syndrome thalamique. Rev Neurol 1906;12:521-532. 12. Dide M, Durocher A: Un cas de syndrome thalamique avec autopsie. Rev Neurol 1904; 12:802-804. 13. Foix C, Hillemand P: Les syndromes de la r\l=e'\gionthalamique. Presse Med 1925;33:113-117. 14. Chinny TA: Sur un cas de syndrome thalamique. Rev Neurol 1904;12:505-511. 15. Duret M: Reserches anatomiques sur la circulation de l'\l=e'\nc\l=e'\phale.Arch Physiol Norm Pathol 1874;6:60-91. 16. Foix C, Hillemand P: Les art\l=e`\resde l'axe enc\l=e'\phaliquejusqu'au dienc\l=e'\phaleinclusivement. Rev Neurol 1925;2:705-739. 17. Lazorthes G, Salamon G: The arteries of the thalamus: An anatomical and radiological study. J Neurosurg 1971;34:23-26. 18. Percheron SMJ: Les art\l=e`\resdu thalamus humain. Rev Neurol 1976;132:297-324. 19. Plets C, DeReuck J, Vander Eecken H, et al: The vasculization of the human thalamus. Acta Neurol 1970;70:687-768. 20. Stephens RB, Stilwell D: Arteries and Veins of the Human Brain. Springfield, Ill, Charles C Thomas Publisher, 1969. 21. Beasley PA, Davenport RW, Nakagawa H: Computerized tomographic localization of the thalamic syndrome: A case report. Comput Radiol 1980;5:427-432. 22. Goto K, Tagawa K, Uemura K, et al: Posterior cerebral artery occlusion: Clinical, computed tomographic, and angiographic correlation. Radiology 1979;132:357-368. 23. Graff-Radford N, Damasio H, Yamada T, et al: Nonhaemorrhagic thalamic infarction. Brain 1985;108:485-516. 24. Takahashi S, Goto K, Fukasawa H, et al: Computed tomography of cerebral infarctions along the distribution of the basal perforating arteries: II. The thalamic arterial group. Radiology 1985;155:119-130. 25. Lapresle J, Haguenau M: Anatomic-clinical correlation in focal thalamic lesions. J Neurol 1973;205:29-46. 26. Foix C, Masson A: Le syndrome de l'art\l=e`\re c\l=e'\r\l=e'\bralepost\l=e'\rieure.Presse Med 1923;31:361\x=req-\ 365. 27. Caplan LR, Hedley-White T: Cuing and memory dysfunction in alexia without agraphia. Brain 1974;97:251-262. 28. Castaigne P, Lhermitte F, Gautier J, et al: Arterial occlusions in the vertebro-basilar system: A study of 44 patients with post-mortem data. Brain 1973;96:133-154. 29. Geschwind N, Fusillo M: Color-naming defects in association with alexia. Arch Neurol 1966;15:137-146. 30. Mohr JP: Posterior cerebral artery, in Bar- nett HJ, Mohr JP, Stein B, et al (eds): Stroke: Pathophysiology, Diagnosis, and Management. New York, Churchill Livingstone Inc, 1986, pp 451-474. 31. Van Buren J, Borke R: The mesial temporal substratum of memory. Brain 1972;95:599-632. 32. Pessin MS, Lathi E, Cohen M, et al: Clinical features and mechanisms of occipital infarction. Ann Neurol 1987;21:290-299. 33. Caplan LR, Hier D, D'Cruz I: Cerebral embolism in the Michael Reese Stroke Registry. Stroke 1983;14:530-536. 34. Gorelick PB, Caplan LR, Hier D, et al: Racial differences in the distribution of posterior circulation occlusive disease. Stroke 1985; Downloaded From: http://archneur.jamanetwork.com/ by a University of Iowa User on 05/29/2015 16:59-64. 35. Pessin MS, Caplan LR, Hedges T: Posterior cerebral artery territory stroke. Curr Concepts Cerebrovasc Dis 1986;21:15-19. 36. Bogousslavsky J, Regli F, Schneider C: Les ramollissements dans le territoire de l'art\l=e`\re Med Hyg 1981;39:3469\x=req-\ c\l=e'\r\l=e'\brale 3478. 37. Pessin MS, Kwan E, DeWitt LD, et al: Posterior cerebral artery stenosis. Ann Neurol post\l=e'\rieure. 1987;21:85-89. 38. Benson DF, Tomlinson EB: Hemiplegic syndrome of the posterior cerebral artery. Stroke 1971;2:559-564. 39. Kuruvilla J, Kramer D, Smatnik L, et al: Posterior cerebral artery occlusion without hemianopia. J Natl Med Assoc 1984;76:509-515. 40. Fisher CM: Pure sensory stroke and allied conditions. Stroke 1982;13:434-447. 41. Kinkle WR, Newman RP, Jacobs L: Posterior cerebral artery branch occlusion: CT and anatomic considerations, in Berguer R, Bauer R (eds): Vertebrobasilar Occlusive Disease. New York, Raven Press, 1984, pp 117-133. 42. Fisher CM: Thalamic pure sensory stroke involving face, arm, and leg. Neurology 1965; 15:76-80. 43. Fisher CM: Thalamic pure sensory stroke: A pathological study. Neurology 1978;28:1141\x=req-\ 1144. 44. Mohr JP, Kase C, Meckler RJ, et al: Sensory motor stroke due to thalamocapsular ischemia. Arch Neurol 1977;34:739-741. 45. Cambier J, Elghozi D, Strube E: Lesions du thalamus droit avec syndrome de l'h\=e'misph\l=e`r\ mineur: Discussion du concept de n\l=e'\gligence tha- lamique. Rev Neurol 1980;136:105-116. 46. Laplane D, Escourolle R, Degos JD, et al: La n\l=e'\gli ence motrice l'origine thalamique. Rev Neurol 1982;138:201-211. 47. Meslam MM: A cortical network for directed attention and unilateral neglect. Ann Neurol 1981;10:309-325. 48. Heilman K, Schwartz H, Watson R: Hypoarousal in patients with the neglect syndrome and emotional indifference. Neurology 1978;28:229-232. 49. Fisher CM: Bilateral occlusion of basilar artery branches. J Neurol Neurosurg Psychiatry 1977;40:1182-1189. 50. Fisher CM, Caplan LR: Basilar artery branch occlusion: A case of pontine infarction. Neurology 1971;21:900-905.