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At least 109 records · Page 6Linked to original sources

Midbrain ptosis caused by periaqueductal infarct following cardiac catheterization: early detection with diffusion-weighted imaging.

Isolated infarcts in the periaqueductal region are rare but have been reported after cardiac catheterization. The authors report a case of dorsal midbrain infarct which caused bilateral ptosis, partial upgaze paresis, and internuclear ophthalmoplegia imaged within eight hours with diffusion-weighted imaging (DWI). The lesion was later confirmed on T2-weighted images. Diffusion-weighted imaging can rapidly confirm the diagnosis of this rare brain-stem infarct.

Blepharoptosis↗

Fatal or severely disabling cerebral infarction during hospitalization for stroke or transient ischemic attack.

Six (1%) of 578 patients admitted for cerebral infarction or transient ischemic attack (TIA) suffered a fatal or severely disabling in-hospital cerebral infarction following a period of stabilization or improvement lasting more than 1 day. These infarctions were characterized by the sudden onset of stupor or coma and subsequent development of transtentorial herniation due to carotid or middle cerebral artery territory infarction, or widespread brain-stem infarction due to basilar occlusion. Only one patient survived. Four patients had large-vessel disease documented by Doppler, angiography, or at autopsy. Each of these six infarcts occurred during the morning hours, 4-9 days after the initial event, 3-8 days after initiation of intravenous heparin, and within 4-8 h after intravenous heparin had been discontinued. No coagulation abnormalities were documented. We believe that these cases indicate that among patients admitted for cerebral infarction or TIA, fatal or severely disabling in-hospital cerebral infarction after a period of stabilization or improvement may occur in patients having an initially mild to moderate clinical deficit, that those suffering large artery disease may be at greater risk, and that there may be a relationship between heparin withdrawal and cerebral infarction in some patients.

Cerebral Infarction↗

Concomitant post-traumatic craniocervical junction epidural hematoma and pontomedullary junction infarction: clinical, neurophysiologic, and neuroradiologic features.

STUDY DESIGN: A case report. OBJECTIVES: To report and discuss a case of post-traumatic epidural hematoma of the craniocervical junction with concomitant brain stem infarction. SUMMARY OF BACKGROUND DATA: Post-traumatic epidural hematoma of the cervical spine and brain stem post-traumatic infarction are very rare disorders. Post-traumatic epidural hematoma is usually located dorsally in the epidural space. METHODS: The clinical, neuroradiologic, and neurophysiologic findings in one patient with post-traumatic epidural hematoma located ventrally at the cervicomedullary junction and associated with medial infarction at the pontomedullary junction are reported. RESULTS: The main clinical finding in this patient was bilateral corticospinal and corticobulbar tract involvement. A magnetic resonance image showed displacement and flattening of the medulla oblongata and of the most cranial portion of cervical cord, which were caused by the epidural hematoma associated with an ischemic lesion of the pontomedullary junction. Results of central motor conduction studies indicated that the abnormality of the central motor pathways was localized at brain stem level, and that there was normal conduction from the cervicomedullary junction to spinal cord. CONCLUSION: This is the first reported case of spinal epidural hematoma located ventrally in the cervical spine at the cervicomedullary junction level and concomitant infarction at the pontomedullary junction resulting from whiplash injury.

Aged↗

[Medial medullary infarct].

Medial medullary infarct is a rare type of brain stem infarction first described in 1908. It was only since the broad use of MRI that an accurate clinical topographical correlation could be documented in survivors. We observed two patients; one of them had an anteromedial unilateral infarction in the upper medulla, and the clinical picture was characterized by contralateral hemiparesis, facial weakness, dysarthria and palatal weakness. The outcome was good. The second patient however showed a severe tetraparesis with only minor brain stem signs, secondary to bilateral anteromedian infarction with a large craniocaudal extension. He survived with severe residual impairment. The most likely cause of infarction was arteriosclerosis of the A. vertebralis and A. spinalis anterior, respectively. These two different cases suggest that the medial medullary syndrome is heterogeneous comprising small unilateral infarctions with mild clinical signs as well as large bilateral infarctions with a poor outcome.

Aged↗

Hemoperfusion in a child who ingested diquat and died from pontine infarction and hemorrhage.

A 2 1/2 year old boy accidentally ingested the herbicide diquat. Progressive neurologic dysfunction preceded his death 143 hours after poisoning. Brain stem infarction and purpura were noted at post mortem and closely resembled the brain stem pathology in 3 of 7 adults who died after diquat ingestion. Renal, gastrointestinal and pulmonary involvement in this child also resembled that seen in adults after ingestion of diquat. Hemoperfusion was performed six times in an effort to lower the body diquat burden. Cellulose-coated, activated charcoal was first employed 40 hours postingestion and removed diquat from serum with clearances of 104 and 39 ml/minute at the initiation of hemoperfusion and 6 hours later, respectively. Serum diquat concentrations decreased rapidly during charcoal hemoperfusion. However, marked rebound in serum diquat concentrations were noted between charcoal treatments, indicating extensive sequestration of diquat by tissues. Thrombocytopenia and hypocalcemia, the major complications of charcoal hemoperfusion, were easily treated. Unlike charcoal, Amberlite XAD-4 resin hemoperfusion did not remove diquat from serum. Charcoal hemoperfusion may temporarily reduce serum diquat concentrations. Whether the early institution and daily performance of charcoal hemoperfusion will minimize diquat-induced damage to brain and other organs is not clear from this case and will only be determined in future studies.

Adolescent↗

Cardiovascular autonomic reflexes in brain infarction.

BACKGROUND AND PURPOSE: Increased sympathetic activity is associated with cardiovascular complications in stroke, but the role of the parasympathetic nervous system has not been carefully outlined. In the present study our purpose was to assess quantitatively autonomic cardiovascular disturbances in brain infarction by measuring cardiovascular autonomic reflexes. METHODS: We studied the autonomic regulation of cardiovascular functions prospectively in 40 patients with brain infarction (acute phase, 1 month, and 6 months) and in 55 healthy control subjects by recording heart rate and blood pressure responses to normal and deep breathing, the Valsalva maneuver, tilting, and isometric work. RESULTS: In the acute phase, heart rate responses to normal breathing, deep breathing, the Valsalva maneuver, and tilting were significantly (P < .05) impaired in both hemispheric and brain stem infarctions, thus indicating hypofunction of the parasympathetic nervous system. At 1 month heart rate responses to normal breathing (brain stem, P < .05), the Valsalva maneuver (brain stem, P < .01), and tilting (hemispheric, P < .05) were still significantly lower than those of the control subjects, but at 6 months significant suppression of the response was found only in tilting (hemispheric, P < .05). CONCLUSIONS: These findings suggest that in addition to the previously well-established sympathetic hyperfunction, brain infarction also seems to cause parasympathetic hypofunction, brain which may be involved in cardiovascular and other known manifestations of autonomic failure associated with stroke.

Adult↗

Complications following acute ischemic stroke.

The objective of this study was to assess typical early-onset complications following ischemic stroke in a large, hospital-based cohort to provide clinical data for future randomized trials and quality standards in clinical routine. 3,866 patients with acute ischemic stroke were prospectively documented in 14 Neurology Departments with an acute stroke unit. Within the first week after admission, increased intracranial pressure (7.6%) and recurrent cerebral ischemia (5.1%) were the most frequent neurological complications. Fever >38 degrees C (13.2%), severe arterial hypertension (7.5%) and pneumonia (7.4%) were the most frequent medical complications. Multivariate regression analysis yielded brain stem infarction and large-artery atherosclerosis as independent predictors for early recurrent ischemic stroke. This study provides representative data on onset and severity of early neurological and medical complications as well as possible predictors for early recurrent cerebral ischemia following acute ischemic stroke.

Aged↗

An MRI analysis of brain-stem and cerebellar lesions and olivary hypertrophy.

We describe the relations between primary brain stem or cerebellar infarct or haemorrhage and secondary inferior olivary pseudo-hypertrophy (OPH). We identified 17 patients (43.6%) among 39 with brain stem or cerebellar vascular disease who had MRI follow-up more than 3 months after their ictus, with OPH. The primary lesions in the 22 cases without OPH were 11 haemorrhages, including 8 medial cerebellar and 3 brain stem lesions, and 11 infarcts: 4 brain stem lesions without accompanying cerebellar involvement, 2 cerebellar infarcts with brain stem extension, and 5 cerebellar lesions without a brain stem infarct. The causative lesion in the 17 patients with OPH included 5 brain stem and 7 cerebellar haemorrhages and 5 brain stem infarcts; no cerebellar infarcts without brain stem involvement were found to cause OPH. Primary involvement of the tegmentum of the brain stem was closely related to secondary OPH, but we could not characterise MRI differences in the cerebellar lesions between the patients with or without OPH.

Adult↗

Don't throw in the towel! A case of reversible coma.

A young woman with pre-eclampsia became unresponsive shortly after delivery. Examination revealed extensive brain stem dysfunction with absent pupillary light reflexes and decerebrate posturing. Computed tomography showed hypodensity throughout the brain stem, and it was initially thought that she had suffered catastrophic brain stem infarction. However, magnetic resonance diffusion imaging and apparent diffusion coefficient mapping showed that she had brain stem vasogenic oedema (posterior reversible encephalopathy syndrome, PRES), rather than cytotoxic oedema. With antihypertensive and supportive treatment, she recovered rapidly, and had no abnormalities on repeat imaging.

Adult↗

Modulation of symptomatic palatal tremor by magnetic stimulation of the motor cortex.

OBJECTIVES: Magnetic stimulation of the motor cortex can be used to determine the involvement of the cortex in rhythmic movement disorders. Symptomatic palatal tremor (SPT) is thought to come from a pacemaker that is relatively resistant to internal and external stimulation. In this study, we investigated the effect of magnetic stimulation of motor cortex on SPT. METHODS: Five male patients, aged 67-79 years, with SPT after brain stem infarction or hemorrhage, all had a synchronous mouth angle twitch with the palatal movement. Electromyographic activity was recorded with a monopolar needle electrode from orbicularis oris. In experiment 1, transcranial magnetic stimulation (TMS) was delivered at 200% motor threshold (MT) to reset SPT. In experiment 2, the effect of TMS intensities was studied at 80-240% MT in two SPT patients. To determine the influence of the TMS, we used the resetting index (RI). RESULTS: TMS reset the tremor in all 5 SPT patients at 200% MT with RIs of 0.86-0.96. The latency of the tremor reappearance after TMS was longer than the pre-stimulus tremor interval, and the intervals between the subsequent tremor bursts were also prolonged. The degree of tremor resetting was closely correlated with the magnetic stimulus intensity and the latency of the tremor reappearance after TMS. CONCLUSIONS: Stimulation of the motor cortex may modulate the generator of SPT.

Aged↗

Cerebral aspergillosis with special reference to cerebrospinal fluid findings.

A case of cerebral aspergillosis in a 69-year-old diabetic man is reported. The disease, initially presenting as headache and vertigo, was caused by Aspergillus fumigatus. Seven CSF specimens were examined. The main findings included decreased glucose and increased protein concentrations, leukocyte reaction and one positive culture for A. fumigatus. Neuropathological examination revealed granulomatous leptomeningitis and typical fungal hyphae. The process probably lasted for more than 1 year and was an important contributing factor to two brain stem infarcts.

Aged↗

[Persistent primitive trigeminal artery presenting with Weber's syndrome: report of a case with three-dimensional CT angiographic evaluations].

We report a rare case of persistent primitive trigeminal artery(PPTA) presenting with brain stem infarction known as Weber's syndrome, and document its unique findings of three-dimensional CT angiography(3 D-CTA). A 69-year-old woman was admitted to our hospital because of gait disturbance and blepharoptosis on the right eye. Neurological examination on admission revealed the right oculomotor nerve palsy, left hemiparesis and dysarthria, all of which indicated the signs and symptoms of Weber's syndrome. Initial CT scan revealed no abnormality, but a subsequent 3 D-CTA demonstrated the PPTA originating from the right internal carotid artery penetrate into the clivus directly to the distal basilar artery, on top of which a small saccular aneurysm was incidentally visualized. Right internal carotid angiograms showed the PPTA run between the cavernous segment of the internal carotid artery and the distal portion of the basilar artery with the filling of both the posterior cerebral and superior cerebellar arteries. However, the proximal portion of the basilar artery was visualized through the right vertebral artery and there was no blood flow to its distal portion. Evidence of infarction was finally confirmed at the right midbrain and thalamus by the MRI performed 5 days after the onset. With a conservative treatment including physical therapy, the patient recovered well from the deficits and could walk by herself with a cane. With regard to the pathogenesis of vertebrobasilar insufficiency in a patient with PPTA, it is generally considered that microembolus from an atherosclerotic carotid artery may be its cause because of the presence of direct communication between the anterior and posterior circulations. In the present case, however, this mechanism may not be applied since there was no evidence of atherosclerotic plaque or stenotic lesions on the carotid arteries. Alternatively, an embolic occlusion may have occurred in the paramedian branches of the posterior cerebral artery since a dilated PPTA itself, which resembled fusiform-aneurysm in appearance, may become the origin of microembolus.

Aged↗

[A case of infarction in brainstem and cerebellum as a initial symptom with bilateral hearing loss].

A 56-year old male presented with a sudden onset of bilateral hearing difficulty. He complained of dizziness and gait disturbance at the onset and subsequently developed bilateral hearing loss and tinnitus. Brain MRI revealed multiple infarcts in bilateral middle cerebellar peduncles, bilateral cerebellar hemispheres and the right cerebral peduncle. Three dimentional computed tomography angiography (3D-CTA) showed severe stenosis of bilateral vertebral arteries. Infarcts were located in the border zone between anterior inferior cerebellar artery (AICA) and superior cerebellar artery (SCA), suggesting hemodynamic infarctions. Auditory brain stem responses (ABR) were recorded three times. The initial ABR demonstrated all waves except for wave I on day 14. Wave I on the left was normal, while wave I peak latency on the right was prolonged. On day 61, all waves were recorded, although peak latencies of waves III to V and interpeak intervals of the wave I to III on the right side were prolonged. Involvements of the cochlear nerve and pontine auditory pathway were suggested from the ABR abnormalities in this case.

Anterior Cerebral Artery↗

Internuclear ophthalmoplegia in tuberculous meningitis.

Two patients with tuberculous meningitis and internuclear ophthalmoplegia are described. Despite treatment with anti-tuberculosis chemotherapy and corticosteroids, both patients died. In one case autopsy showed severe basal meningitis with diffuse brain stem infarction secondary to widespread vasculitis.

Adult↗

Fluid-attenuated inversion recovery (FLAIR) for assessment of cerebral infarction. Initial clinical experience in 50 patients.

BACKGROUND AND PURPOSE: Our aim was to evaluate fluid-attenuated inversion recovery (FLAIR) sequence in the diagnosis of cerebral infarction with MRI. METHODS: A retrospective review was undertaken of 50 consecutive MRI studies ordered for suspected cerebrovascular accident. All studies included FLAIR and rapid acquisition with relaxation enhancement (RARE) T2-weighted spin-echo sequences. The two sequences were compared independently by four observers at two different institutions. Detectability of lesions and image quality were scored. RESULTS: Overall, FLAIR sequences proved superior in 10 patients, detecting acute cortical infarcts missed with RARE spin-echo technique in five patients. In five additional patients, improved characterization of chronic infarction and improved detection of microangiopathic deep hemispheric changes were observed. One brain stem infarct was missed with the FLAIR sequence. CONCLUSIONS: FLAIR offers advantages in detection of acute infarcts affecting the cortical ribbon, is a useful, rapid adjunct to conventional T2-weighted spin-echo sequences, and has the potential to replace these in the future.

Artifacts↗