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Two cases of spontaneous cerebral ventriculostium are presented. The first case is that of a 3 year-old girl with a thumb-sized soft scalp tumor of the occipital region (dural hypertrophy) and hydroencephalodysplasia (Picaza). PVG revealed noncommunicating hydrocephalus with asymmetrical deformity of the lateral ventricle and agenesis of corpus callosum (Fig. 1). Ventriculoatrial shunt was performed. Three years passed under the useful life when she readmitted to our clinic complaining headache, nausea and vomiting. On the first hospital day she fell into respiratory arrest accompanied with coma after the tonic convulsion, and eventually, she died on the fourth hospital day. Postmortem examination revealed spontaneous cerebral ventriculostium which communicated with the posteromedial trigone of the left lateral ventricle (Fig. 3). Combined other malformations such as dysgenesis of the corpus callosum and only one anterior cerebral artery, etc. were found. The second case is that of a young adult, a 22 year-old male with rapidly progressing intracranial hypertension. PVG revealed marked dilatation of the lateral and the third ventricle, non-filling of the aqueduct and spontaneous cerebral ventriculostium which communicated with the posterior part of the third ventricle (Fig. 4). And insidiously he fell into akinetic mutism. After suboccipital exploratory craniotomy and ventriculo-peritoneal shunt akinetic mutism improved gradually, and he was discharged on foot after 7 months. PEG performed on June 8, 1973, showed no evidence of aqueduct obstruction and injected air passed from the fourth ventricle to the third one smoothly. He lives on now under a useful condition. These 2 cases are the first report on literatures in Japan, but presumably there must be many other cases. Since W. H. Sweet reported his own two cases of spontaneous cerebral ventriculostium on 1940, more than thirty cases have been published on literatures. However, there are found various expressions to describe the same condition (Table 1). We would like to propose that the most suitable expression is "ventriculostium" not only in deference to the originality of W. H. Sweet but also not to confuse this pathogenetic state with other similar conditions. The author's next interest is the chronological fact that from W. H. Sweet (1940) to A. Torkildsen (1948), all but one ostiums reported situated at the posteromedial trigone of the lateral ventricle, whereas after A. Torkildsen, they were found at the posterior part of the third ventricle in many cases. The reason is unknown. It would appear that three main conditions are necessary for the development of ventricluostium just beneath the tentorium. The first, there must be increased pressure within the lateral or the third ventricle. The second essential feature is the lack of any large space occupying lesion in the the infratentorial space. The third, there must be wider space between the tentorial incisura and the brain stem.
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PMID:[Spontaneous cerebral ventriculostium (author's transl)]. 94 70

We studied five patients with cerebral hemorrhage limited to the head of the caudate nucleus. This rare localization represents 11% of central nuclei hemorrhages. This entity has various clinical expressions; some are similar to a subarachnoid hemorrhage, others show the same manifestations associated with hemiparesis and neuropsychological findings, while still in others, the neuropsychological syndrome with speech, behaviour or memory disturbances predominates. Recovery depends on the patient's previous clinical status and on the presence of associated lesions at the time of hemorrhage. Typical warning signs, like headache, are often absent in the elderly and debilitated. Meningismus is explained by the intraventricular extension of the hemorrhage. Motor deficit, usually moderate, is probably due to impairment of the anterior portion of the posterior arm of the internal capsule. Destruction of the head of the left caudate nucleus, which is part of the circuit causing "subcortical aphasias", is responsible for non specific speech disturbances, that are however remarkably rich in semantic paraphasias. These dysfunctions could be caused by a "cortical diaschisis" as suggested by SPECT analysis. Memory dysfunction as a result of caudate lesion is questioned. However confusion and behavioural disturbances, like preservations, transitory mutism and self neglect, seem characteristic. As shown by cerebral blood flow (CBF) studies, these disturbances might represent a frontal dysfunction caused by the interruption of the dorso-latero-prefrontal and orbito-frontal circuits. When the hemorrhage extends beyond the head of the caudate nucleus, behavioural changes occur due to the involvement of neighbouring structures such as the thalamus, internal capsule, temporal lobe and nucleus accumbens. Caudate hemorrhages occur mostly in the elderly, often with long-standing arterial hypertension causing lesions of the lenticulo-striate arteries. Severe stenosis or complete occlusion of the middle cerebral artery with a fragile anastomotic circuit or angiopathies in younger individuals (particularly Asiatics: moyamoya disease) are less frequent, but they should be considered and investigated by arteriography. Vascular malformations are a rare cause and a relationship with amyloid angiopathy can only be suspected.
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PMID:[Hematoma of the head of the caudate nucleus]. 229 Oct 35

Infarction in the territory of the anterior choroidal artery (AchA) has been the subject of several recent reports. To the classical clinical syndrome of hemimotor, hemisensory, and visual field deficit has been added hemiataxia acute pseudobulbar mutism, pure motor and pure sensory syndromes and disorders of higher cortical function. The definition of anatomic and clinical correlates to AchA stroke is aided by CT-MRI findings and reveals an unexpected superior extension of infarct to include the periventricular caudate nucleus and inferior corona radiata. Prognosis depends upon unilaterally, bilateral strokes having often a fatal outcome. Etiology and treatment may be intimately related to hypertension.
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PMID:A new view of anterior choroidal artery territory infarction. 306 61

Pseudobulbar mutism is rarely attributed to bilateral discrete posterior limb internal capsule-medial globus pallidus infarction. Few cases of bilateral anterior choroidal (AchA) artery territory infarction have been reported. We present 8 patients with ischaemic stroke in this location and vascular distribution who have a characterizable syndrome. All had the abrupt onset of inability to speak, swallow or phonate, accompanied by varying degrees of facial diplegia, hemiparesis, hemisensory loss, lethargy, neglect and change in affect. The appearance of clinical signs depends upon the presence of a new infarct contralateral to an older lesion in mirror position. The pathogenesis and progression of neurological deficit appears to be intimately related to hypertension. The role of intrinsic intracranial vascular pathology related to diabetes mellitus, embolism of cardiac origin and atherosclerosis is currently undefined. The prognosis for recovery is poor. Half of our patients died within a year of onset of symptoms. Capsular pseudobulbar mutism is recognized by the abrupt appearance of neurological deficit consistent with internal capsular pathology and is confirmed by CT scan or MRI.
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PMID:Acute pseudobulbar mutism due to discrete bilateral capsular infarction in the territory of the anterior choroidal artery. 338 10

A clinicopathologic study was made of 45 elderly persons whose autopsied brains showed the pathologic changes of progressive subcortical vascular encephalopathy (Binswanger type). Progressive subcortical vascular encephalopathy (PSVE) was observed in 3.8 per cent of all autopsied brains of elderly persons and in 6.7 per cent of the brains of those with cerebrovascular diseases. White matter lesions were graded from I to III (slight to severe). Small infarcts in the basal ganglia, thalamus, and pons were common, but the cerebral cortex was usually preserved. Neuropsychiatric symptoms included dementia, urinary incontinence, hemiplegia, pseudobulbar palsy, psychosis, parkinsonism, and mutism. In thge Grade III group there was a high incidence of pseudobulbar palsy, parkinsonism, and mutism. Pathologic study showed marked cerebral arteriosclerosis in almost all cases. Angionecrosis was observed in 60 to 80 per cent. Fibrotic and stenotic changes of the blood vessels in the deep white matter were also noted, particularly in 90 per cent of the Grade III cases. A suggested explanation for the pathogenesis of PSVE is based on the effects of various complications such as hypertension, cardiac disease and malnutrition which may play an important role in PSVE when they occur in elderly persons with a history of long-standing hypertension, marked cerebral arteriosclerosis, and arteriolar changes in the cerebral white matter.
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PMID:Clinicopathologic study of progressive subcortical vascular encephalopathy (Binswanger type) in the elderly. 709 54

A 65 years old woman with chronic high blood pressure and diabetes mellitus presented with a mutism akinetic of sudden onset and a right total hemiplegia with a Babinski sign secondary to a left anterior cerebral artery infarction. She had had six months earlier a transient gait disturbance. At that time, the CT scan showed lacunar infarcts of the head of both caudate nuclei. Neuropathological examination revealed that the left infarction of the anterior cerebral artery involved the superior frontal gyrus, the supplementary motor area, the cingulate gyrus and the corpus callosum. There were also multiple lacunes of the head of both caudate nuclei, anterior limb of the internal capsules, white matter, basal ganglia and thalami. The mutism akinetic was thought to be the result of a bilateral disruption of a functional loop including on each side, the supplementary motor area, the cingulate gyrus, the subcallosal tract and the head of the caudate nucleus. On the right side, the lesion of the caudate nucleus could have interrupted this loop normally involved in the induction of voluntary movements and in the communication with the external surroundings.
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PMID:[Akinetic mutism with right hemiplegia caused by infarction in the territory of the left anterior cerebral artery]. 876 28

We reported a 67-year-old woman with bilateral caudate head infarcts. She developed sudden mutism followed by abulia. She was admitted to our hospital 2 months after ictus for further examination. She showed prominent abulia and was inactive, slow and apathetic. Spontaneous activity and speech, immediate response to queries, spontaneous word recall and attention and persistence to complex programs were disturbed. Apparent motor disturbance, gait disturbance, motor aphasia, apraxia and remote memory disturbance were not identified. She seemed to be depressed but not sad. Brain CT and MRI revealed bilateral caudate head hemorrhagic infarcts including bilateral anterior internal capsules, in which the left lesion was more extensive than right one and involved the part of the left putamen. These infarct locations were thought to be supplied by the area around the medial striate artery including Heubner's arteries and the A1 perforator. Digital subtraction angiography showed asymptomatic right internal carotid artery occlusion. She bad had hypertension, diabetes mellitus and atrial fibrillation and also had a left atrium with a large diameter. The infarcts were thought to be caused by cardioembolic occlusion to the distal portion of the left internal carotid artery. Although some variations of vasculature at the anterior communicating artery might contribute to bilateral medial striate artery infarcts, we could not demonstrate such abnormalities by angiography. Bilateral caudate head infarcts involving the anterior internal capsule may cause prominent abulia. The patient did not improve by drug and rehabilitation therapy and died suddenly a year after discharge.
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PMID:[Bilateral caudate head infarcts]. 950 74

We present a case study of a 46-year-old woman with a psychotic depressive illness of 2 months' duration with the coexisting medical diagnoses of critical aortic stenosis, severe labile hypertension, renal failure necessitating hemodialysis of 7-years' duration, and systemic lupus. Because of unresponsiveness to an antidepressant drug regimen, severe motor retardation, mutism, and refusal of food and fluids by mouth, an urgent indication for electroconvulsive therapy (ECT) was established. However, the patient refused ECT, and to allow its initiation, a court order was obtained. In view of the coexisting diagnoses of critical aortic stenosis, labile hypertension, and renal failure, ECT represented a substantially increased risk in this patient because of severe arterial hypertension and tachycardia. The patient was successfully managed during each ECT, using a combination of metoprolol by mouth, which was supplemented by i.v. esmolol immediately prior to the application of the ECT stimulus, and sodium nitroprusside, which was infused for several minutes prior to the seizure and thereafter to attenuate arterial hypertension. Nevertheless, sudden death, a well-known complication of critical aortic stenosis, occurred 96 hours after the fourth ECT.
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PMID:Hemodynamic responses to ECT in a patient with critical aortic stenosis. 1073 32

We describe the unusual case of a 63-year-old woman with a history of arterial hypertension who presented a sudden weakness of the lower limbs followed by mutism, akinesia and dyspraxia. Magnetic resonance images showed a bilateral medial frontal infarction. Digital subtraction angiography documented a right azygous anterior cerebral artery with severe stenosis in its sub-callosal tract; the left anterior cerebral artery showed mild hypoplasia with only sub-frontal and fronto-polar branches. No embolic source was documented. Afterwards the patient presented a gradual and partial recovery of both motor and cognitive functions.
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PMID:Bilateral medial frontal infarction in a case of azygous anterior cerebral artery stenosis. 1093 47

We report a 72-year-old right-handed man who was diagnosed as having crossed aphasia. He had polycythemia, hypertension and an old cerebral infarction in the right occipital lobe. He was admitted to our hospital because of muscle weakness in the left extremities at the age of 71. In the laboratory data, red blood cells(689 x 10(4)/microliter) and platelets(87.6 x 10(4)/microliter) were increased in number. Brain CT detected a right putaminal hematoma and an old infarct in the occipital lobe on the right. After admission, he developed non-fluent speech, and impairments of auditory comprehension, writing and naming due to the infarction in his right cerebral hemisphere including the middle cerebral artery distribution. The standard language test of aphasia(SLTA) revealed marked impairments in the language function, except for reading kana and kanji words. This writing was severely impaired compared with other language dysfunctions. Auditory comprehension, repetition and reading were impaired at the sentence level rather than at the kana word level. Furthermore, he suffered from left hemiparesis and left unilateral spatial neglect. We diagnosed his impairments of language function as crossed aphasia based on his right-handedness, CT findings and the results of SLTA. His language center was considered to be located in both cerebral hemispheres. Compared with typical findings in reported cases of crossed aphasia, the presence of both non-fluent speech and mutism were consistent with previous observations. However, the marked impairments of auditory comprehension, repetition and naming were different. Polycythemia and hypertension were considered to be the risk factors of cerebral infarction in our patient.
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PMID:[A case of crossed aphasia in a dextral patient with polycythemia]. 1199 62


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