Anantha N. Manepalli

Solitary Intramedullary Neurosarcoidosis: Role of MRI in Early Detection

Background. Intramedullary neurosarcoidosis may be the first manifestation of the disease and may mimic a tumor clinically and radiographically. Two patients who presented with cervical intramedullary lesions on magnetic resonance imaging (MRI) scans were found to have neurosarcoidosis. Clinical presentation. Two patients with negative past medical history presented with progressive myelopathic features, and intramedullary cervical lesions were detected on MRI scan; the diagnosis was made on biopsy of the lesions. Early therapeutic intervention led to a favorable outcome. Conclusion. Intramedullary neurosarcoidosis, especially in the cervical cord, can be the initial presentation of the disease, mimicking a tumor. MRI scan, biopsy, and, in fewer cases, angiotensin‐converting enzyme levels can help with the diagnosis and may lead to a favorable outcome.

Epidural Hematoma Producing Brown-Sequard Syndrome: A Case Due to Ruptured Hemangioma with Magnetic Resonance Imaging Findings

A man developed spontaneous spinal epidural hematoma secondary to ruptured hemangioma with a clinical picture resembling acute partial Brown‐Sequard syndrome. Diagnosis by magnetic resonance imaging (MRI) allowed prompt surgical decompression and complete reversal of the neurological deficits. The diagnosis, etiology, and MRI findings of spinal epidural hematomas are discussed.

Hyperdense Basilar Artery An Early Computed Tomography Sign of Thrombosis

Noncontrast computed tomographic scans (CT scans) may show a hyperdense basilar artery before a brainstem infarct is visualized. This early sign should assist clinicians in confirming the diagnosis of basilar artery thrombosis. In a review of admission records of 750 patients with acute cerebrovascular disease from July 1991 to June 1993, at Saint Louis University Hospital, 20 patients were identified with clinical signs of nonlacunar, vertebrobasilar distribution infarction. Eight of these had pontomesencephalic ischemia. Their neuroimaging studies and medical records were evaluated. Four patients with acute clinical signs of pontomesencephalic infarction were found to have a hyperdense basilar artery on CT scans. The scans of 2 patients were excluded because of dolichoectasia; in the other 2 patients, the basilar artery appeared normal on the CT scan. The hyperdense basilar artery was detected within the early hours of neurological symptoms and often was the only detectable abnormality on the scan. In 3 patients extensive brainstem infarcts subsequently developed and they died. Basilar artery thrombosis was confirmed by pathological study in all these patients. In the fourth patient basilar artery occlusion and a large pontine infarct were evident by magnetic resonance imaging and angiography. A hyperdense basilar artery is a common feature on CT scans of patients presenting with an early clinical diagnosis of thrombosis. Untreated, the hyperintense basilar artery often portends a poor prognosis. Its ready recognition should guide further interventional studies and treatment.

Unusual hemorrhage with use of synthetic dural substitute : MR findings

Delayed hemorrhage is an unusual complication of silastic dural substitute that can have a prolonged latent period. Two such patients that presented 6 and 12 years following surgery and that were evaluated by MR imaging are reported.

Infantile Alexander's disease: serial neuroradiologic findings.

Serial neuroimaging studies in Alexanders disease were obtained on an African-American girl who died at 4z\x years of age. She presented with macrocephaly, psychomotor retardation, spasticity, a seizure disorder, and hydrocephalus. A thorough metabolic evaluation of defined leukodystrophies, including Krabbes disease, adrenoleukodystrophy, metachromatic leukodystrophy, Canavans disease, and Leigh disease, was negative. A diagnosis of Alexanders disease was made based on the clinical features and ruling out all other possible causes. It was confirmed by pathologic findings of numerous subpial, subependymal, and perivascular Rosenthal fibers throughout the entire cerebrum. Interestingly, autopsy also identified the stenotic sylvian aqueduct owing to Rosenthal fiber accumulation, explaining the origin of hydrocephalus. The evolution of magnetic resonance imaging findings appears to be unique in this disease. (J Child Neurol 2002;17:463-466).

Association between brain tissue pH and brain injury during asphyxia in piglets.

BACKGROUND Acidosis may contribute to brain injury from asphyxia, but its role is unclear. In order to evaluate the association between brain acidosis and cerebral injury, we subjected piglets to hypoxia and hypotension (HYP-HOTN) or hypoxia alone (HYP) to inflict varying amounts of brain damage. We hypothesized that piglets with a more severe brain injury would have a lower brain pH. METHODS Piglets had a pH microprobe inserted into the cerebral cortex. HYP animals breathed 5-8% O(2)/7% CO(2) for 30 min with mean arterial pressure (MAP) maintained at >40 mmHg. HYP-HOTN animals breathed the same gas for 30 min, but during the last 15 min, MAP was reduced to 25-30 mmHg by withdrawing blood. After 4 h of recovery, the animals were perfusion-fixed and pathology assessed. Somatosensory-evoked potentials (SEP) were also monitored. RESULTS HYP-HOTN piglets had more neuropathology than HYP animals. During the last 15 min of injury, brain pH in the HYP-HOTN group was significantly higher than that in HYP. However, recovery of brain pH was prolonged in the HYP-HOTN animals. The amount of time for brain pH to recover to > or =7.00 correlated very well with both the degree of neuropathology and SEP recovery. The reduction in brain pH, either absolute or relative to baseline, was not associated with the severity of damage. CONCLUSIONS The time needed for brain pH to recover after asphyxia, but not its severity, was associated with the amount of brain injury. Further study is warranted to determine whether immediate restoration of brain pH will reduce brain damage.

Correlation of Brain Tissue pH With Histopathology in a Piglet Model of Perinatal Asphyxia † 821

Asphyxia causes acidosis which may potentiate neural injury. We hypothesized that hypoxia & hypotension cause lower brain pH and more severe neural injury than hypoxia alone. METHODS: Anesthetized piglets (age 0.05). Brain & serum pHs did not differ in either group (p>0.05). SEP recovery in HTN (6.3± 3.3% of baseline) was less than (p 0.05) over time. Brain and serum pH correlated (p<0.0001) in all groups. HTN pathology had severe neuronal necrosis; HYP pathology was much less severe. CONCLUSIONS: Brain & serum pH are similar with HYP& HTN. The pH changes do not correlate with pathology & SEP recovery. The results indicate that brain pH is not associated with neuropathology.Supported by the Fleur-de-Lis Foundation.

Recurrent Syncope and Quadriplegia

A 72‐year‐old man had posturally induced syncopal episodes, followed by quadriparesis, coma, and death. Neuroimaging studies supported the clinical diagnosis confirmed by neuropathological findings.