Sensorimotor Stroke Due to Thalamocapsular Ischemia J. P. Mohr, MD; Carlos S. Kase, MD; Roy J. Meckler, MD; C. M. Fisher, MD \s=b\A 61-year-old hypertensive diabetic man awoke with a numb, heavy right arm and leg; symptoms progressed within 30 hours to a dense right hemisensory syndrome involving head, face, trunk, arm, and leg, accompanied by a right hemiparesis, involving tongue, face, arm, and leg with extensor plantar response, leaving him barely able to move the arm and leg against gravity. No impairment in alertness, memory, language, praxic, or visual functions was evident at any time. Improvement in motor function began in 24 hours and progressed to walking status by discharge on day 23. Eight days passed before the sensory deficit showed improvement, and it was still prominent at discharge. Autopsy three months later showed a 4 x 2 x 4-mm lacune in the ventral poste- rior nucleus of the left thalamus, with a of pallor on stained microscopic sections extending into the immediately adjacent posterior limb of the internal zone capsule. This case appears to be unique in that a sensorimotor stroke has been produced by a confirmed thalamocapsular infarct. (Arch Neurol 34:739-741, 1977) Accepted for publication June 27, 1977. From the Stroke Service and the Charles S. Kubik Memorial Laboratory of Neuropathology, Massachusetts General Hospital and Harvard Medical School, Boston. Reprint requests to Stroke Service, Massachusetts General Hospital, Boston, MA 02114 (Dr Mohr). Although several different types of ±\. lacunar syndromes have already been described,1 the present case marks the first reported instance, to our knowledge, in which two types have occurred from a single infarct in an autopsied case. The anatomic data is of further interest, as it suggests at least some degree of arterial supply common to contiguous anatomic struc¬ tures hitherto thought always to be supplied independently. REPORT OF A CASE A 61-year-old right-handed, hyperten¬ sive, diabetic man with no prior stroke history awoke in the early morning hours with numbness of the right arm and leg. He walked easily to a friend's car, and noted right-sided weakness only after a 30minute ride to a local hospital. The sensory deficit steadily progressed over the next hour to involve the entire right side. The weakness progressed only slightly during that time. He was referred for further evaluation. Personal examination at the Massachu¬ setts General Hospital seven hours after onset disclosed a deficit confined to a right-sided sensorimotor abnormality. Weakness only faintly affected the face and tongue; arm elevation was limited to 50 cm for only two seconds; the grip was barely detectable; the leg elevated only 2 cm for five seconds; a feeble ipsilateral extensor plantar response and normal stretch reflexes were demonstrated. Cerebellar testing was impaired by the hemiparesis, but was not abnormal otherwise. Downloaded From: http://archneur.jamanetwork.com/ by a New York University User on 06/20/2015 no detection of was virtually pinprick, touch, vibration, or passive move¬ ment of skin and joints in the right arm and leg, face, ear, side of the neck, axilla, There and lateral trunk. Sensation shaded toward normal near the midline of the trunk. He was unable to name objects placed in the hand and passively manipulated with assist¬ ance from the examiner. He was slightly dysarthric. Detailed testing disclosed no abnormalities in language, memory, pic¬ ture description, spelling, repeating aloud, visual fields, extraocular movements, ste- reognosis of the left hand, and left-sided sensorimotor function. No bruits were heard in the neck. The optic fundi were normal. Blood pressure was 140/90 mm Hg. Within two hours, with the patient under continuous observation, the right arm and leg became steadily worse, reaching a state of virtually complete paralysis. The dysarthria also worsened slightly. No further intensification or spread of the sensory deficit occurred. The deficit was un¬ changed for 18 hours. Thirty hours after onset, strength of the right leg had improved sufficiently to permit the ex¬ tremity to be elevated 5 cm for eight seconds. Lumbar puncture demonstrated an opening pressure of 17 cm of water; CSF was slightly blood-tinged, with 10,600 RBCs per cubic millimeter. No xanthrochromia was observed. The protein level was 70 mg/100 ml. A left carotid arteriogram revealed no abnormalities. Radionuclide brain scan and electroencephalogram were normal. On the third day, the leg could be mesencephalon. The pattern of the vessels supplying the base of the brain was sketched and photographed, with the plan of later tracing the arterial source of the lacunar infarcì to its parent cerebral, or even Horizontal section of left cerebrum, stained for myelin, showing thalamic lacune and pallor in adjacent internal capsule. elevated 5 cm for ten seconds, and the arm 25 cm for 50 seconds, but no change was evident in the sensory deficit. On the sixth day, the strength had improved enough to allow the patient to sit unassisted on the side of the bed, but no change in sensation was found and hypesthesia of the entire scalp bilaterally was noted. Reexamination on the eighth day showed further improve¬ ment in strength, and also in awareness of pinprick over the trunk almost to normal levels as compared with the unaffected left side. The deficit in sensation in the right arm and leg had improved slightly. A residual dense band of hypesthesia ex¬ tended from the right axilla to the hip. This vertical trunk band persisted into the third week, during which time the sensorimotor deficit elsewhere faded to the point that stereognosis of the right hand was normal, and pinprick over the right extremities was reported only slightly reduced. The patient walked easily, and his grip and arm elevation were overcome only with consid¬ erable effort. Subsequent examinations disclosed only faint residua of the syndrome, including the axillary to hip band. The patient died suddenly three months after onset of his stroke, while complaining of severe chest pain. Pathologic Findings On horizontal brain section, the single significant abnormality noted was a 4 2 4-mm lacune located in the ventral posterior nucleus of the left thalamus (Fig¬ ure). The lacune was transected on a single horizontal section through the specimen. The lower portion of the gross specimen was then trimmed in the coronal and sagittal planes to yield a block size suitable for gapless horizontal serial sections from the site of the gross horizontal section downward through the cerebrum all the way to the subarachnoid space below the Downloaded From: http://archneur.jamanetwork.com/ by a New York University User on 06/20/2015 choroidal, artery. The microscopic serial sections were studied in detail, and all arteries and veins in the region of the lacune visible within the field of a scanning lens were traced through the depth of the specimen. Remarkably, the small arteries within the lacune were found to become progressively smaller as the lacune was followed down¬ ward, until they completely disappeared. The artery within the lacune appeared not to enter it from below as a larger vessel and become progressively smaller above as expected, but the reverse. No evidence of segmental fibrinoid necrosis2 was observed to account for the narrowed lumen. On the assumption that the arterial supply entered the lacune from above the site of gross horizontal section, hitherto not observed in lacunar studies, the brain sections rostral to the gross horizontal sections were also studied. Unfortunately, this block had been fixed and sectioned for celloidin, so as to show the entire horizontal section of brain containing the lacune. Cerebral tissue at this interface had there¬ fore been lost in the sections made for celloidin. Detailed analysis failed to show the arterial pattern to the lacune. The lacune lay in the thalamus,' not in the internal capsule. On myelin stain, the capsule adjacent to the thalamic lacune was pale. No infarct necrosis was evident; the clear zone of infarct necrosis lay wholly within the thalamus. No arterial supply common to the lacune and the adjacent pallor was obvious. COMMENT A thalamic infarct with pallor in the adjacent capsule has produced a senso¬ rimotor syndrome hitherto unrecog¬ nized, to our knowledge, as a type of lacunar stroke. Lacunar syndromes from individual infarcts recorded to date1 include pure motor stroke, pure sensory stroke dysarthria-clumsy hand syndrome, homolateral ataxia and crural paresis, and, from multiple lacunar infarcts, the lacunar state. Lacunar infarcts have proved common, representing 18% of strokes in the Harvard Cooper¬ ative Stroke Registry of 850 prospectively studied cases. Pure motor stroke is by far the most common. To our knowledge, until the present case, no sensorimotor stroke from a single pathologically confirmed lacunar in¬ farct has been described. The combined syndrome in the present case followed a temporal course and severity of deficit com¬ monly experienced separately in cases of pure motor and sensory stroke. Taken separately, the sensory and motor deficits each seemed typical for the types of deficit met in lacunar stroke. Of interest considering the thalamic infarct and capsular pallor, the sensory component slightly pre¬ ceded the motor and outlasted it. Neither the sensory nor motor deficit fully faded clinically with time, but both underwent considerable im¬ provement. No special features apart from the coexistence of sensory and motor deficit stamped this case as distinguishable from other sensori¬ motor strokes without visual field, extraocular motility, language, or be¬ havior disorders. Pure sensorimotor stroke is com¬ monly referred to clinically, but uncommonly encountered when indi¬ vidual cases are analyzed in detail. Other clinical deficits in behavior, language, extraocular motility, or visual fields usually are discoverable and assist in the diagnosis. In the Harvard Stroke Registry, "pure" sen¬ sorimotor stroke has been associated with hematoma, embolism, and atherostenosis and occlusion of the major extracranial arteries, as well as with lacune. Until the syndrome is more thoroughly defined, it would be pre¬ mature to assign a lacunar cause to the majority of sensorimotor strokes. The case further bears on the arterial supply to the thalamus and adjacent internal capsule. To date, it has been claimed that the supply to the two structures lies in wholly different cerebral arterial territories. The thalamus has been considered to receive its principal supply from the posterior cerebral artery and a lesser supply from choroidal arteries.4 The capsule has been thought to be supplied entirely from lenticulostriate arteries, the posterior limb of the capsule bordering on the thalamus, by the lenticulostriates from the middle cerebral artery.5 Both the thalamic and the capsular supply have been described as arcuate-penetrating. Save for the faint possibility of joint supply to the thalamus and capsule, suggested in the figures illustrating a recent publication6 but not in the text itself, the present case provides new evidence suggesting that the thal¬ amus and at least some portion of the capsule may share a common blood supply. This investigation was supported in part by grants NS 10828-A1-S1 and HS 00188 from the National Institutes of Health. References 1. Fisher CM: Cerebral ischemia-less familar types. Clin Neurosurg 18:267-336, 1971. 2. Fisher CM: The arterial lesions underlying lacunes. Acta Neuropathol 12:1-15, 1969. 3. Fisher CM: Pure sensory stroke involving face, arm and leg. Neurology 15:774-784, 1965. 4. Percheron SMJ: Etude anatomique du thalamus de l'homme adulte et de sa vascularisation arterielle, thesis, Paris, 1966. 5. Plets C, DeReuck J, Vander Ecken H, et al: The vascularization of the human thalamus. Acta Neurol Belg 70:685-767, 1970. 6. Percheron SMJ: Les arteres du thalamus humain. Rev Neurol 132:297-324, 1976. New Requirement for Authors.—Congress recently passed The Copyright Revision Act of 1976, effective January 1, 1978, which affects the American Medical Association's procedure for reviewing of manuscripts submitted for publication. In view of this law, all transmittal letters accompanying manuscripts submitted for publication, should contain the following language: "In consideration of the AMA taking action in reviewing and editing my submission, the author(s) undersigned hereby transfers, assigns, or otherwise conveys all copyright ownership to the AMA in the event that such work is published by the AMA." Downloaded From: http://archneur.jamanetwork.com/ by a New York University User on 06/20/2015