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PubMed1998

Cognitive impairment in young adults with infratentorial infarcts.

OBJECTIVE: To describe cognitive functions and functional outcome in young patients with isolated infratentorial infarcts. BACKGROUND: Contemporary knowledge implies a cerebellar contribution to cognitive behavior. Neuropsychological examination of patients with selective cerebellar lesions provides an opportunity to document the existence and nature of clinically relevant cognitive manifestations from lesions of the cerebellum. METHODS: Prospective case series. The patients were assessed acutely and at 4 and 12 months after onset. Twenty-four patients from a consecutive series of 105 patients aged 18 to 44 years with cerebral infarction had a brain stem or cerebellar infarction. Fourteen age-matched controls were used for neuropsychological comparisons. Evaluation included MRI, angiography, and transesophageal echocardiography. Disability and neurologic dysfunction were assessed by the modified Rankin scale, NIH stroke scale, and maximal working capacity. A comprehensive neuropsychological battery was performed at baseline in 20 of the 24 patients. RESULTS: Eighteen patients had a cerebellar infarct. Two patients had lateral medullary infarcts, and two isolated pontine infarcts. Twenty-two patients had a favorable outcome according to the modified Rankin scale (grade 0-2) and the NIH scale. In contrast, 12 patients were granted full or partial sick leave at the 4 months follow-up, and 10 patients at 12 months. Patients generally performed worse than controls in various aspects of cognitive function, especially in tasks concerning working memory, the temporary storage of complex information, and cognitive flexibility. Measures of verbal IQ (r = -0.74) and performance IQ (r = -0.78) were related to the size of the infarct. The block design task performance in the early poststroke period predicted maximal working capacity at 12 months. CONCLUSIONS: Cerebellar damage impairs central aspects of attention and visuospatial skills. In contrast, intelligence and episodic memory remain unchanged. When the lesion involves large portions of the cerebellar hemispheres, changes concerning broad areas of intelligence may occur. The prognosis is favorable for neurologic dysfunction, but cognitive deficits may prevent return to work.

Adolescent↗
PubMed1990

[Edematous cerebellar infarction. A clinico-pathological study of 16 cases].

Sixteen cases of cerebellar infarction with brain stem compression and tonsillar herniation were studied post-mortem. None was operated. Cardiac embolism was the most common cause (75% of the cases). Infarction involved the superior cerebellar artery territory in 8 cases, and multiple cerebellar artery territories (including in each case the posterior inferior cerebellar artery territory) in 8 cases. It involved the cerebellum only in 10 cases. In the 6 other cases, it was associated with an infarct in the paramedian territory of the brain stem. The oedematous swelling was linked to the large size, the rostral site and the embolic causes of the infarct. Cases with massive infarction of the brain stem differed from others by severe motor weakness of the limbs in 5 cases and a deep coma in the 6th. On the contrary, only one of the 10 cases with lone cerebellar infarct had a mild hemiparesis. Thus, when a hemi- or tetraplegia occurred in the course of an oedematous cerebellar infarction, an associated massive paramedian infarction of the pons must be suspected rather than a brain stem compression. This can be taken into account when a surgical treatment is discussed.

Arteries↗
PubMed1991

Central nervous system infarction related to cocaine abuse.

BACKGROUND: Cocaine use in the United States has reached epidemic proportions, and increased availability of "crack" since 1983 has noticeably increased the incidence of neurovascular complications. In this report, we examine the relationship between cocaine use and ischemic infarct. SUMMARY OF COMMENT: This study reports 18 cases of ischemic cerebrovascular events, which occurred among 15 men and three women aged 21-47 years who were evaluated in a 2-year period. Clinical presentations include thirteen cases with hemispheric infarcts, two brain stem strokes, two anterior spinal artery infarcts, and one with both hemispheric and cerebellar infarcts. Nine patients smoked crack, four snorted cocaine, and three injected it intravenously. In two cases, the route of administration could not be determined. Two patients died, but the other survived with various degrees of neurological deficit. CONCLUSIONS: Traditional risk factors for strokes were identified in only six patients, suggesting that these factors are not necessary for the occurrence of a cocaine-related infarct. Multiple overlapping mechanisms may be responsible, including vasospasm, sudden onset of hypertension, myocardial infarction with cardiac arrhythmias, increased platelet aggregation, and vasculitis.

Adult↗
PubMed2001

Abduction paresis with rostral pontine and/or mesencephalic lesions: Pseudoabducens palsy and its relation to the so-called posterior internuclear ophthalmoplegia of Lutz.

BACKGROUND: The existence of a prenuclear abduction paresis is still debated. METHODS: In a retrospective design, we identified 22 patients with isolated unilateral (n = 20) or bilateral (n = 2) abduction paresis and electrophysiologic abnormalities indicating rostral pontine and/or mesencephalic lesions. Another 11 patients had unilateral abduction paresis with additional ocular motor abnormalities indicating midbrain dysfunction. Eight of these 11 patients also had electrophysiological abnormalities supporting this location. Electrophysiological examinations in all patients included masseter and blink reflexes (MassR, BlinkR), brainstem auditory evoked potentials (BAEP), and direct current elctro-oculography (EOG). RESULTS: Unilateral MassR abnormalities in patients with unilateral abduction paresis were seen in 17 patients and were almost always (in 16 of 17 patients) on the side of the abduction paresis. Another 11 patients had bilateral MassR abnormalities. BlinkR was always normal. EOG disclosed slowed abduction saccades in the non-paretic eye in 6 patients and slowed saccades to the side opposite to the abduction paresis in another 5 patients. Re-examinations were done in 27 patients showing normalization or improvement of masseter reflex abnormalities in 18 of 20 patients and in all patients with EOG abnormalities. This was always associated with clinical improvement. CONCLUSIONS: Electrophysiologically documented or clinically evident rostral pontine and/or mesencephalic lesions in our patients exclude an infranuclear intrapontine 6th nerve lesion and indicate the existence of an abduction paresis of prenuclear origin. An increased tone of the antagonistic medial rectus muscle during lateral gaze either by abnormal convergence or impaired medial rectus inhibition seems most likely.

Abducens Nerve Diseases↗
PubMed1978

[Pseudo-tumoral softening of the cerebellum].

The author establish an onerall picture of cerebellar infarction with brain stem compression after reviewing 63 cases published in the literature and 4 personal observations. The frequency of this affection can be compared with that of cerebellar hematomas. Diagnosis is based on its predominance in males, the early age at which it appears, its rapid and typical onset, and the delayed signs of brain stem compression. Conventional neuroradiological procedures show an expanded cerebellar volume, and the scanner can specify the ischaemic nature of the lesion. As soon as changes in consciousness occur surgical decompression is necessary, first by external drainage of C.S.F. and later, if necessary, by direct access to the postdrior fossa.

Adult↗
PubMedDate not supplied

[Top of the basilar artery syndrome: clinico-radiological aspects of 25 patients].

UNLABELLED: INTRODUCTION, PATIENTS AND METHODS: We studied 25 patients, 16 women and 9 men (average age 64.8 years; SD 8.6; range from 36 to 79 years) admitted to our hospital with clinical findings compatible with obstruction at the level of the bifurcation of the basilar artery. The patients were selected on clinical and neuroradiological criteria. RESULTS AND CONCLUSIONS: All patients included in the study had presented with two or more infarcts in the vertebro-basilar territory, related to pathology of the rostral region of the basilar artery. Diagnosis was confirmed on CT and MRI. Infarcts were found in the thalamus, brain-stem, cerebellum and parieto-occipital lobe. Infarct of the thalamus associated with another infarct in a different region was the most frequent lesion. The CT-MRI findings in the 25 cases were: 14 patients had unilateral thalamic infarcts associated with another infarct. There were 4 patients with bilateral thalamic infarcts and 5 with bilateral occipital infarcts. In 11 patients the occipital infarct was associated with another infarct at a different level, and 6 patients each had a cerebellar infarct together with a brain-stem infarct. In 12 patients the lesions were localized to three or more areas. The commonest clinical manifestations were: motor deficit (68%), abnormal eye movements (48%), cerebellar dysfunction (40%), alteration of the level of consciousness (32%), visual field defects (20%), pupil anomalies (16%). The risk factors most frequently associated were: arterial hypertension (64%), a history of cerebrovascular accident (28%), smoking (28%), diabetes mellitus (24%) and atrial fibrillation (20%). Mortality was 8%. Unlike the classical descriptions, motor deficit was the most frequent symptom in our series.

Adult↗
PubMed2005

Brainstem vascular stroke anatomy.

Brainstem infarcts comprise approximately 10% of all first ischemic brain strokes. The extrinsic vascular supply to the stem is complex. The intrinsic vascularization of the stem may be conceptualized in terms of four relatively constant and distinct vascular territories designated anteromedial, anterolateral, lateral, and dorsal (or dorsolateral). The anatomic structures found within each intrinsic territory determine the symptomatology associated with infarction of that territory. This territorial anatomy permits the knowledgeable physician to plan an MR imaging examination tailored to the patient's history and to predict the patient's neurologic deficits from the MR imaging findings.

Brain Stem↗
PubMed2006

Cluster breathing associated with bihemispheric infarction and sparing of the brainstem.

OBJECTIVE: To report cluster breathing pattern associated with a nonbrainstem lesion. DESIGN: Case report. SETTING: Neurointensive care unit, St Mary's Hospital, Rochester, Minn. PATIENT: A patient with subarachnoid hemorrhage developed severe, diffuse, distal bilateral middle cerebral artery vasospasm with resultant cortical laminar necrosis and transient cluster breathing. Intervention Magnetic resonance imaging revealed bihemispheric lesions but no brainstem lesion. CONCLUSION: Cluster breathing may occur with nonbrainstem lesions.

Aged↗
PubMed2005

Claude's syndrome associated with supranuclear horizontal gaze palsy caused by dorsomedial midbrain infarction.

Claude's syndrome caused by dorsal midbrain lesion is characterized by ipsilateral third nerve palsy and contralateral ataxia. To date, reports in the literature concerning Claude's syndrome associated with the midbrain paresis of horizontal gaze are rare. A 62-year-old man suddenly developed left third cranial nerve palsy, right lateral gaze palsy, and right ataxia. Intact Bell's phenomenon and preserved right horizontal oculocephalic reflex suggested the lateral gaze palsy in the right eye was supranuclear in nature. Magnetic resonance imaging (MRI) revealed an infarction in the left dorsomedial midbrain. Although the red nucleus has often been suggested as the lesion site responsible for Claude's syndrome, a lesion of the superior cerebellar peduncle just below and medial to the red nucleus could be responsible for this syndrome. This case demonstrates neurological heterogeneity of midbrain infarction.

Ataxia↗
PubMed2002

[A case of the persistent vegetative state following symmetrical peduncular infarction].

A 64-year-old woman presented with sudden onset of disequilibrium and dysarthria. Two days later she became lethargic and tetraparetic. An emergency MRI disclosed multiple infarctions in the medulla oblongata and pons. An angiogram revealed severe stenosis of the rostral basilar artery. The patient underwent a rapidly progressive course with impaired consciousness and flaccid tetraplegia. MR images 7 days after the onset disclosed a symmetrical midbrain infarction that was localized mainly in the cerebral peduncles, suggesting a distal basilar artery occlusion as the cause of this pathology. Since 4 weeks after the onset the patient was in the persistent vegetative state, which was essentially unchanged during the 1-year follow-up period. Persistent vegetative state is known to be caused by diffuse supratentorial or bilateral thalamic lesions, but in our case the lesions were restricted to the infratentorial area. We speculate a mechanism to cause the persistent vegetative state by partial impairment of the connection to the thalamic ascending system or extrathalamic ascending system, which leads to the dissociation of arousal(preserved in this case) and awareness(impaired in this case) after the ventral midbrain infarction.

Brain Stem Infarctions↗