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PubMedDate not supplied

Ataxic-hemiparesis, localization and clinical features.

Five additional cases of ataxic-hemiparesis are reported. In 3 cases, computed tomography showed an area of decreased attenuation in the posterior limb of the internal capsule, and in 1 case, 2 areas of attenuation in the corona radiata. A review of previously reported cases suggest that brainstem ataxic-hemiparesis may be separated from supratentorial forms of ataxic-hemiparesis by the presence of nystagmus, dysarthria, cranial neuropathy, and the absence of sensory abnormality.

Aged↗
PubMedDate not supplied

CT-CBF correlations of cognitive deficits in multi-infarct dementia.

Fifteen right-handed patients with Multi-Infarct Dementia underwent cognitive testing by the Jacobs Mini-Mental Scale (MMQ), and xenon contrast CT scanning. Local cerebral blood flow (LCBF) and local partition coefficient (L lambda) values were measured by stable xenon contrast CT scanning and potential methodological errors were discussed. Reduced values were graded: 0 = normal, 1 = mild, 2 = moderate, 3 = severe. Graded values were pooled and plotted on composite brain maps to display locations of abnormal L lambda and LCBF values. Topographic brain maps, showing most frequent locations of reduced L lambda values, confirmed the common anatomical locations of multiple cerebral infarcts to be distributed in both thalami, temporal lobes, basal ganglia, left internal capsule and right cingulate cortex. Gray matter flow values were reduced in similar cortical and subcortical regions. There were no correlations between MMQ scores and reduced LCBF values for caudate and lenticular nuclei. Direct and statistically significant correlations were found between reduced MMQ scores and mean LCBF values for left or right frontal cortex, left or right temporal cortex and left or right thalamus. Subgrouping MMQ tests according to functions assessed, indicated that left mid-temporal ischemia correlated with dyscalculia and memory disturbances while ischemia of both frontal lobes correlated with disorientation to time and place.

Aged↗
PubMedDate not supplied

Effect of small deep hemispheric infarction on the ipsilateral cortical blood flow in man.

The effect of small, deep ischemic lesions on the ipsilateral cortical circulation was investigated in 10 patients with persistent mild or moderate neurological deficits due to infarcts in the internal capsule. rCBF studies by the 133Xe intracarotid injection method were performed 14-180 days after the onset of the infarction. The rCBF functional image was made up from the data of 133Xe dynamic images measured by an Anger-type gamma camera and the rCBF values were calculated by the initial slope method. The average value of mean rCBFs (mCBF) in 10 patients was 44.9 +/- 7.1 ml/100g/min (average PaCO2; 39.9 +/- 4.3 mm Hg). In the rCBF functional images, a focal hypoperfusion area was observed in all cases and localized around the central sulcus, especially in the precentral and central areas. Significant decreases of mCBF and the tendency to decrease of the rCBFs in the hypoperfusion focus were noted in the patients with the larger infarcts in comparison with those with the smaller ones. These results suggest that a small, deep ischemic lesion such as a capsular infarct may have remote effects on the ipsilateral cortical circulation, due probably to the damage of a number of fibers passing through the lesion.

Adult↗
PubMedDate not supplied

Lacunar syndrome due to intracerebral hemorrhage.

It has been recognized that small intracerebral hemorrhage not uncommonly produced lacunar syndromes. In this study, we examined cases of intracerebral hemorrhage presenting as lacunar syndromes. Of 174 cases with recent intracerebral hemorrhage, 19 presented with a lacunar syndrome: 4 presented with pure motor hemiparesis, 5, ataxic hemiparesis, 3, dysarthria-clumsy hand syndrome, 7, sensorimotor stroke, and, none, pure sensory stroke. The sites of hemorrhage were capsular in 11, putamenal in 6, and pontine in 2. In these 19 patients, 17 were hypertensive, and the signs characteristic of parenchymal hemorrhage, e.g., gradual onset, headache, nausea, vomiting and stiff neck, were absent or very rare. Computed tomography revealed that one third of the patients had one or more non-symptomatic lacunae in the basal ganglia, the corona radiata or the anterior limb of the internal capsule. These observations suggests that hypertensive intracerebral hemorrhage causes lacunar syndrome more often than previously considered and is apt to manifest ataxic hemiparesis and sensorimotor stroke. Computed tomography is the only way of differentiating hemorrhagic "lacunar" syndrome from lacunar infarct.

Ataxia↗
PubMedDate not supplied

Somatosensory evoked potentials in pure sensory stroke and related conditions.

Somatosensory evoked potentials were reviewed for their correlation with CT scan and clinical features of ischemic "pure sensory stroke" and "pure sensorimotor stroke". Somatosensory evoked potentials were normal in all 11 cases of pure sensory stroke, and CT was normal in ten. The N2-P2 components of the somatosensory evoked potentials were abnormal in all 4 cases of pure sensorimotor stroke, and all had low density CT lesions in the lateral thalamus and/or posterior limb of the internal capsule. It is concluded that somatosensory evoked potentials and CT scans are routinely abnormal in pure sensorimotor stroke, but they are consistently normal in pure sensory stroke, and should not be interpreted as evidence against a clinical diagnosis of pure sensory stroke.

Adult↗
PubMedDate not supplied

Perforating branches of the middle cerebral artery. Microanatomy and clinical significance of their intracerebral segments.

Perforating branches of the middle cerebral arteries (MCA) were examined on the forebrain hemispheres of fourteen human brains. It was noticed that their intracerebral segments arose from the MCA main trunk, and its terminal and collateral (cortical) branches. They terminated in certain parts of the basal ganglia and internal capsule. The course, direction, shape, diameters and branches of these segments were examined in detail. Classification of all the vessels was made according to caliber. It was concluded that the size of lacunar infarcts depends on the caliber and ramification zone extent of the occluded perforating vessels. Diameters of the intracerebral segments of vessels ranged from 80 to 840 microns, of their terminal branches from 80 to 780 microns, and of the collateral branches from 50 to 400 microns. The average size of the ramification zone was: 41.6 X 15.5 mm for the entire perforating artery; 37.9 X 15.5 mm for the intracerebral segment; 23 X 13 mm for the terminal branches; 8.9 X 5.5 mm for larger collateral branches; and 2.6 X 1.4 mm for the smallest branches.

Adult↗
PubMedDate not supplied

Progressive lacunar infarction with demonstrated patency of the middle cerebral artery.

Two cases of progressive hemiplegia were closely followed by daily clinical examination. In both, the CT scan and CSF were normal on admission. In both, objective aggravation occurred in three or more steps over four days, progressing from minor finger clumsiness to total paralysis of the arm. In both cases a second CT scan a day after appearance of hemiplegia demonstrated a lacune in the corona radiata just above the internal capsule. In one case an intravenous digital subtraction angiogram demonstrated patency of the middle cerebral artery during the course of the progression. In the other case, serial study with transcranial Doppler ultrasound documented the continued patency of the middle cerebral artery. These two cases demonstrate that it is not necessary to postulate transient occlusion of the middle cerebral artery as an essential mechanism for progressive lacunar infarction.

Aged↗
PubMedDate not supplied

Evaluation of brain dysfunction in hypertensive putaminal hemorrhage with multimodality evoked potentials.

Changes in multimodality evoked potentials (MEP's), consisting of somatosensory evoked potentials (SEP's), visual evoked potentials (VEP's), and auditory evoked brainstem responses (AEBR's), were studied in 36 patients with hypertensive putaminal hemorrhage to ascertain the relation among areas and distribution of brain dysfunction, the size of hemorrhage on computerized tomographic scan, and the clinical outcome. Among MEP's, SEP's were most significantly involved in all patients. Abnormalities in VEP's and AEBR's remained mild or moderate when the hemorrhage did not extend to the diencephalon. If SEP's were normal or mildly abnormal, they improved early the ictus. These patients did well clinically. If SEP's were absent, the patients had poor outcome even when the hemorrhage was small and located outside the internal capsule. In contrast, deterioration or persistence of MEP's indicated secondary insult to the brain and poor patient outcome. Early and serial MEP studies are useful in evaluating primary and secondary brain dysfunction and in predicting patient outcome in hypertensive putaminal hemorrhage.

Adult↗
PubMed1988

Pure motor hemiplegia secondary to a saccular basilar artery aneurysm.

Pure motor hemiplegia is the most commonly encountered lacunar syndrome and is classically associated with small infarctions in the contralateral internal capsule or basis pontis. Pure motor hemiplegia has also been observed secondary to a wide variety of other vascular and nonvascular focal central nervous system processes. We describe a patient with pure motor hemiplegia associated with a saccular basilar artery aneurysm causing a lacunar infarction of the cerebral peduncle.

Aged↗
PubMed1989

Blood velocity in the middle cerebral artery and regional cerebral blood flow during carotid endarterectomy.

Blood flow velocity in the middle cerebral artery, determined by transcranial Doppler ultrasonography, was monitored during 31 carotid endarterectomies. Electroencephalogram (EEG) was also monitored, and regional cerebral blood flow (rCBF) was measured. The relation between rCBF and mean velocity was dependent on the rCBF level; the correlation was strong if rCBF was less than 20 ml/100 g/min but weak if rCBF was greater than that level. Ipsilateral EEG suppression was related to a rCBF threshold of 9 ml/100 g/min and to a mean velocity threshold of 15 cm/sec; the rCBF threshold was more specific for EEG change. Postischemic hyperemia was evident in measurements of mean velocity but not of rCBF. These disparities between mean velocity and rCBF seemed to be due to three factors: 1) disproportionately high mean velocity in patients with stenosis of the middle cerebral artery, 2) a nonlinear relation between mean velocity and rCBF, and 3) the anatomically different regions of the brain in which mean velocity and rCBF are measured. The velocity measurement appeared to be relatively more sensitive than rCBF to hemodynamic events in the corpus striatum and internal capsule.

Aged↗
PubMed1989

Corticofugal axonal degeneration in rats after middle cerebral artery occlusion.

We used the Fink-Heimer method to study degenerating corticofugal axons after unilateral middle cerebral artery occlusion in 14 adult male Long-Evans hooded rats. Axonal degeneration in the pyramidal tracts was prominent at 1-3 weeks, manifesting in well-defined silver-impregnated axonal bundles coursing from the internal capsule to the pyramids and crossing completely to the contralateral spinal cord. In half of eight rats examined at 1-3 weeks, the cortical infarct included the forelimb region of the sensorimotor cortex, and degenerating corticospinal axons could be traced to the lower cervical segments; in rats with involvement of the hindlimb cortical area as well, axonal degeneration extended to the lumbosacral segments. Terminal degeneration products were present in the forebrain, midbrain, and brainstem within 2 days after arterial occlusion; the number of degenerating terminals peaked at 7 days and decreased gradually thereafter up to 6 weeks. Dense terminal degeneration was observed in the trigeminal nuclear complex of all seven rats studied at 2 and 7 days. In these seven rats, five had small cortical infarcts, and silver-impregnated terminals were observed in the lateral reticular formation; in two rats with large cortical lesions, terminal degeneration was prominent in the medial reticular formation as well. We conclude that infarcts produced by middle cerebral artery occlusion cause axonal degeneration in the brainstem and spinal cord. The Fink-Heimer method may be useful for evaluating the rat middle cerebral artery occlusion model.

Animals↗
PubMed1989

Nicardipine reduces ischemic brain injury. Magnetic resonance imaging/spectroscopy study in cats.

We investigated whether the calcium channel entry blocker nicardipine would reduce ischemic brain damage in barbiturate-anesthetized cats subjected to permanent unilateral occlusion of the middle cerebral artery. The evolution of cerebral injury was assessed in vivo in 24 cats by a combination of proton magnetic resonance imaging and phosphorus-31 magnetic resonance spectroscopy for 5 hours following occlusion. Immediately thereafter, the volume of histochemically ischemic brain tissue was determined planimetrically in triphenyl tetrazolium chloride-stained serial coronal sections. Nicardipine was initially administered as an intravenous bolus injection of 10 mg/kg/hr 15 minutes before or 15 minutes after occlusion, followed by continuous infusion at 8 mg/kg/hr for the 5 hours of the experiment. Compared with untreated controls, cats that received nicardipine before or after occlusion showed a significant reduction in the extent of edema in the ipsilateral cerebral cortex, internal capsule, and basal ganglia. The results of phosphorus-31 magnetic resonance spectroscopy studies suggest that nicardipine may protect against cerebral ischemic damage by an action on cellular metabolic processes that preserve high-energy phosphates during the ischemic period.

Animals↗
PubMed1989

Sarcoidosis presenting with stroke.

A 25-year-old black man with sarcoidosis presented with transient ischemic attacks followed by sudden, persistent right hemiparesis. He gave a history of recent, recurrent lower motor neuron facial palsy. Computed tomography demonstrated an infarct in the left internal capsule. Chest x-ray film showed bilateral hilar and mediastinal lymphadenopathy and multiple opacities in the lung fields. Serum angiotensin converting enzyme concentration was raised, and a Kveim test was positive for sarcoidosis. Despite clear pathologic reports of cerebral vasculitis in neurosarcoidosis, the occurrence of stroke is extremely rare.

Adult↗
PubMed1989

Selective platelet deposition during focal cerebral ischemia in cats.

Platelet deposition in the microcirculation may play a role in focal cerebral ischemia. We investigated platelet deposition in selected parts of the cat brain after temporary middle cerebral artery occlusion. Ten anesthesized cats were given autologous indium-111-labeled platelets and chromium-51-labeled erythrocytes. The right middle cerebral artery was occluded with miniature aneurysm clips for 3 hours via a transorbital approach; blood pressure was reduced concomitantly to decrease the collateral circulation. Removal of the clips initiated a 45-minute period of normotensive reperfusion. After sacrifice, the brain was removed and sectioned for comparison of right- versus left-hemisphere platelet deposition. Platelets were selectively deposited in the territory of the occluded right middle cerebral artery. Significant deposition was found in the caudate nucleus, internal capsule, parietal cortex, and the centrum semiovale. Our findings support the evidence that platelets are deposited in the microvasculature during temporary severe focal cerebral ischemia.

Animals↗
PubMed1989

Hypesthetic ataxic hemiparesis in a thalamic lacune.

Right hemiparesis with an ipsilateral hypesthesia and ataxia developed in a 57-year-old man. Magnetic resonance imaging showed a left thalamic lacune bordering the medial portion of the posterior limb of the internal capsule. This finding implicated some pathogenetic mechanism of ataxic hemiparesis.

Ataxia↗
PubMed1989

Prevalence of silent stroke in patients presenting with initial stroke: the Framingham Study.

It is common to find computed tomography scan evidence of prior stroke without a history of such an event. The frequency, risk factors for, and relevance of silent strokes are unknown. The Framingham cohort of 5,184 men and women aged 30-62 years and free of stroke at entry to the study have been followed with periodic examinations since 1950. We studied the silent strokes found on computed tomography scan of all initial strokes that occurred between January 1, 1979, and July 31, 1987. During these 8 1/2 years, 164 initial strokes occurred; 124 had computed tomography scans performed. There were 13 (10%) with silent stroke, 71 had abnormalities related to their presenting acute stroke, and 40 had normal computed tomography scans. There were 15 silent lesions; eight were lacunar infarcts in the basal ganglia-internal capsule area, seven were small cortical infarcts. Glucose intolerance was the sole risk factor that occurred significantly more frequently (11 of 13) in the group with silent lesions (p less than 0.04) than in the group with computed tomography evidence of acute stroke. Silent stroke is not rare; it was present in at least 10% of acute initial stroke patients arising in a general population. The relation of these silent lesions to the development of "vascular" dementia and poststroke disability deserves further study.

Cerebral Infarction↗
PubMed1989

Deafferentation versus cortical ischemia in a rabbit model of middle cerebral artery occlusion.

A two-site middle cerebral artery occlusion model in rabbits was developed. Platinum electrodes served for simultaneous recordings of regional cerebral blood flow, auditory evoked potentials, and electroencephalogram in the left and right auditory cortex and in the left medial geniculate body. Auditory evoked potentials and regional cerebral blood flow were also recorded in the subcortical white matter, and regional cerebral blood flow was recorded in the internal capsule. Distal segment occlusion of the middle cerebral artery caused severe cortical ischemia in four of 11 rabbits (Group I), accompanied by abolition of the auditory evoked potential in the left auditory cortex and white matter and severe reduction of the left electrocorticogram. Deep subcortical regions were affected either little or not at all. In the remaining seven rabbits (Group II) with only mild disturbance of cortical perfusion after distal middle cerebral artery occlusion, additional clamping of the proximal middle cerebral artery stem reduced thalamocortical tract blood flow and abolished cortical auditory evoked potentials. Spontaneous electrocorticogram was less affected in Group II than in Group I; thalamic regional cerebral blood flow and auditory evoked potentials were not altered. Histologically, ischemic lesions predominated in the cortex of Group I and in the subcortical structures of Group II rabbits. While correlated reductions in regional cerebral blood flow and auditory evoked potentials indicate effective cortical ischemia, the impairment of auditory evoked potentials in Group II rabbits must be due to cortical deafferentation by ischemia in the afferent tract. This model permits the investigation of the effects of predominantly cortical or subcortical ischemia in one functional system.

Afferent Pathways↗
PubMed1990

Denervation in hemiplegic muscles.

This study examined the frequency of denervation activity in hemiplegic muscles in relation to the size and location of the central lesion. We studied 20 patients, 14 with major unilateral cerebral infarctions in the middle cerebral or internal carotid territories; four with a single lacune in the pons, internal capsule, or thalamus; and two with precentral infarcts. Using somatosensory evoked potentials, motor conduction studies, and assessments of conduction across the plexus and roots, we detected no conduction abnormalities on the affected side. Fibrillation was common in both groups, especially in distal and intermediate muscles. The distribution of the fibrillation and the normal conduction studies suggested that trauma of peripheral nerves was not a factor. Although the normal conduction studies and pattern of fibrillation activity do not exclude peripheral nerve trauma as the cause of the fibrillation, we suggest that transsynaptic degeneration is a reasonable alternative explanation.

Action Potentials↗