Sensorimotor Stroke Due to Thalamocapsular Ischemia

F isher designated the syndrome of weakness and pyramidal signs on one side combined with an ipsilateral cerebellar-like ataxia as ataxic hemiparesis.1 In several subsequent reports, the upper pons, posterior limb of the internal capsule, corona radiata, midbrain, thalamus, and parietal lobe have been demonstrated as sites of the lesions.1 -10 Since the classic thalamic syndrome was first described by Dejerine and Roussy, 11 a few cases of ataxic hemiparesis from contralateral thalamic lesions have been reported. 7 - 91213 We report a case of hypesthetic ataxic hemiparesis with a lacunar infarct in the contralateral thalamus as seen on magnetic resonance imaging (MRI). Case ReportA 57-year-old man was admitted to Seoul National University Hospital for a poorly controlled blood sugar level. He did not smoke or drink, but the patient had been suffering from diabetes mellitus for 5 years. His blood pressure was 140/90 mm Hg, and diabetic retinopathy was detected in both fundi. The rest of his neurologic examination, other than a moderately impaired vibratory sensation in both feet and hypoactive deep tendon reflexes, was normal. While his electrocardiogram and serum albumin level (3.9 g/dl) were normal, proteinuria (1103 mg/day) and glucosuria were detected. His fasting and 2-hour-postprandial blood glucose levels were 222 and 322 mg/dl, respectively. This high blood glucose level was controlled with an oral hypoglycemic agent.In the evening of the 14th hospital day when he was preparing for a stroll, a tingling sensation suddenly developed in his right arm and leg, folFrom the Department of Neurology, College of Medicine, Seoul National University, Seoul, Korea.Address for reprints: Hojin Myung, MD, Department of Neurology, Seoul National University Hospital, 28, Yunkeun-dong, Chongno-Ku, Seoul 110-744, Korea.Received October 11, 1988; accepted December 27, 1988. lowed by weakness and clumsiness in his right hand. On examination he was alert and welloriented with a normal neuropsychological assessment. There was a mild right-sided weakness of his involved limbs mainly in his arm, but no facial weakness was observed. Heel-to-shin and great toe-to-finger tests showed a marked ataxia on the right side, and the patient had some difficulty in accomplishing the finger-to-nose test due to a mild dysmetria. Impairment in rapid alternate movements of his right limbs and in the vibratory sensation and joint position of his right hand and foot were elicited, while touch and pain sensations were reduced by 40-50% in his right trunk, arm, and leg and on the right side of his face. As observed previously, on the left side only the vibratory sensation of his foot was reduced. Sensation approached normal near the midline of his trunk. On walking, the patient staggered and nearly fell to his right, but no cerebellar tremor or truncal ataxia were evident. His tendon reflexes remained symmetrically decreased, but his right plantar response was extensor. A brain computed tomogram taken approximately 15 hours later (Figure 1) show...

supporting

confidence: 91%

Hypesthetic ataxic hemiparesis in a thalamic lacune.

Lee

Roh

Myung

1989

“…29 Later clinicians clarified the clinical findings in patients with pontine infarction related to basilar artery occlusion 30 ; patients with cerebellar infarction at various loci in the cerebellum [31][32][33][34][35] ; midbrain, thalamic, and occipital and temporal lobe infarction in patients with embolism to the "top-of-the-basilar" artery 35,36 ; and patients with small localized infarcts in the pons, medulla, and thalamus caused by disease of the penetrating artery supply. 35,[37][38][39][40][41][42][43][44][45][46] …”

Section: Clinicoanatomic Correlationsmentioning

confidence: 99%

Posterior Circulation Ischemia: Then, Now, and Tomorrow

Caplan

2000

171

103

know and appreciate where we are now and where we are going in the future, it is essential to know where we have been. We cannot afford to relive and repeat the history of stroke every several decades. Posterior circulation stroke represents a microcosm of stroke in general. In this presentation I first review the development of ideas regarding brain and posterior circulation ischemia and its recognition and treatment. I then share some recent data from a large prospective registry of patients with posterior circulation ischemia. Finally, I look ahead to reflect on what I believe should be the future directions for research and for the care of patients with posterior circulation disease.Patients who present to physicians and hospitals with symptoms that suggest posterior circulation ischemia are handled differently from patients who have symptoms that suggest anterior circulation disease in the great majority of medical facilities in the United States and in the world. A patient who has an attack of dizziness with diplopia and ataxic gait usually has a brain image but seldom has vascular or cardiac investigations. A diagnosis of "vertebrobasilar insufficiency" (VBI) is often made, and physicians then debate whether or not to treat with warfarin-type anticoagulants, and, if so, for how long and at what intensity. In contrast, a patient who has right-hand weakness and aphasia is usually evaluated and treated quite differently at the very same facilities. Brain imaging, cardiac investigations, noninvasive vascular tests of the carotid and intracranial anterior circulation with the use of extracranial and transcranial ultrasound and/or MR angiography (MRA) and CT angiography, and catheter angiography are often pursued, depending on the local technological capabilities and experience of the treating physicians. An effort is made to identify the etiology and mechanism of the ischemia. Treatment is then chosen among a variety of possibilities (including carotid artery surgery, angioplasty, anticoagulants, and antiplatelet aggregants) depending on the nature, location, and severity of the occlusive disease and the mechanism of ischemia.Why should anterior and posterior circulation ischemia be handled so differently? Does this schizophrenic approach make sense? After all, the internal carotid artery and its branches and the vertebral (VA) and basilar arteries (BA) and their branches are just a few inches apart; they are made of the same coats and look the same under the microscope except for size. These vessels carry the same blood under the same blood pressure. The diseases that affect the blood vessels in the 2 circulations are the same. Do stroke mechanisms really differ between the 2 circulations? How did this differing approach originate, and does it continue to make sense today? These are some questions that I will attempt to answer as I review the development of ideas about posterior circulation ischemia and as I report recent data. Development of IdeasHerein I review how knowledge about the posterior circulation ...

“…As only 12 of our patients had MRI, which is more sensitive than CT for detecting posterior fossa Previous reports have inconsistently correlated neuroimaged, autopsy-proven, and clinically inferred abnormalities localized to the thalamus, internal capsule, and corona radiata with the hypesthetic ataxic hemiparesis symptom complex. Mohr et al 39 attributed a sensory motor deficit to infarction in the posterolateral thalamocapsular region. Discrepant accounts of thalamic involvement in reports of hypesthetic ataxic hemiparesis may be due to the insensitivity of CT for depicting infarction in gray matter nuclei such as the thalamus, as well as to the fact that various anatomic sites of destruction may lead to similar neurologic deficits.…”

Section: Landaumentioning

confidence: 99%

Capsular hypesthetic ataxic hemiparesis.

Helgason

Wilbur

1990

Twenty-three patients with hypesthetic ataxic hemiparesis underwent computed tomography or magnetic resonance imaging. Twenty-two patients had infarcts of lacunar or slightly larger size in the contralateral posterior limb of the internal capsule. In 15 patients the infarct extended superiorly into the adjacent paraventricular region, and in seven it extended into the lateral thalmus. In eight patients the infarct was limited to the posterior limb of the internal capsule, and in only two patients was an ipsilateral to capsular pontine lacune found. Despite a location similar to that of pure motor and pure sensory lacunar stroke, hypesthetic ataxic hemiparesis correlates with larger infarcts, most often located in the posterior medial superior territory of the antierior choroidal artery. Some infarcts appeared to be localized immediately posterolateral to this region, in the posterior cerebral artery territory. The presence and extent of infarction is better detected by the addition of magnetic resonance imaging to computed tomography. (Stroke 1990;21:24-33)