Short latency afferent inhibition associated with cortical compression and memory impairment in patients with chronic subdural hematoma.

OBJECTIVE: To evaluate the cortical excitability in patients with mild cortical compression. METHODS: The present study used short interval intracortical inhibition (SICI), intracortical facilitation (ICF), and short latency afferent inhibition (SAI) to evaluate motor cortex excitability in 16 chronic subdural hematoma (CSDH) patients with memory impairment and compared the data with those of 16 healthy controls. RESULTS: SAI was reduced in patients compared with controls (99±14 vs. 47±11% of the test size; p<0.0001, unpaired t-test). CSDH patients tended to have a high resting motor threshold and less pronounced SICI and ICF than controls, but these differences were not significant. Treatment of hematoma improved memory impairment and SAI in CSDH patients with wide individual variations that ranged from an increase of 74% to 17% of test size. CONCLUSION: These findings suggest that measuring SAI may provide a means of probing the integrity of cortical cholinergic networks in a compressed human brain.

Cerebral vasculitis associated with amyloid angiopathy: case report.

A 78-year-old female presented with coexisting primary angiitis of the central nervous system (CNS) and cerebral amyloid angiopathy (CAA) manifesting as motor aphasia caused by a left frontal lobe lesion. Magnetic resonance imaging revealed an enhanced lesion with moderate surrounding edema.Technetium-99m propylene amine oxime single-photon emission computed tomography showed decreased cerebral blood flow (CBF) in the lesions, and high serum soluble-interleukin-2 level was detected, suggesting intravascular lymphoma of the CNS. Cerebral biopsy revealed CAA with secondary florid vasculitic appearance. The CBF and neurological symptoms, such as aphasia and dementia, recovered following steroid treatment. Cerebral vasculitis associated with CAA should be included in the differential diagnosis of an unusually enhanced lesion, because timely diagnosis and aggressive treatment are critical to successful recovery in such elderly patients.

A hemispherotomy for intractable startle epilepsy characterized by infantile hemiplegia and drop attacks.

Startle epilepsy is provoked by unexpected sensory stimuli, mainly auditory, and reveals subsequent tonic posturing of the limbs. We present a case of intractable startle epilepsy with infantile hemiplegia and discuss the indications for a hemispherotomy.

Possible involvement of interferon beta in post-operative vasculitis restricted to the tumour bed: a case report.

Cerebral vasculitis is a very rare complication after brain tumour surgery. We herein report a case and discuss the origins of this complication. A 52-year-old female was admitted because of motor aphasia due to a left frontal lobe brain tumour. The magnetic resonance imaging (MRI) study revealed a non-enhanced tumour. A partial resection of the tumour and the placement of an Ommaya's reservoir were performed. The pathological diagnosis was an oligoastrocytoma. The patient recovered well without any neurological deficits. Post-operative radiotherapy and the intravenous injection of interferon beta were performed. During these treatments, the patient showed a continued high fever. An MRI scan revealed multiple enhanced lesions in the residual tumour, thus raising suspicions about a post-operative infection. We therefore performed a tumour biopsy and the removal of the exogenous materials. The histopathological diagnosis was vasculitis in the residual tumour. The patient's consciousness and neurological symptoms recovered quickly with the steroid treatment. Following the radiotherapy (50 Gy total), complete remission of the tumour was rapidly obtained and no recurrence was observed. Cerebral vasculitis confined to the tumour bed is an unusual complication; however, this special condition was of critical importance for a successful tumour regression in this patient.

Neuroprotective and antiamnesic effect of donepezil, a nicotinic acetylcholine-receptor activator, on rats with concussive mild traumatic brain injury.

In this study we evaluated the effect of donepezil on the neurodegeneration and behavioral impairments induced by mild traumatic brain injury (MTBI). Donepezil is an acetylcholinesterase inhibitor that is used to treat Alzheimer's disease. Donepezil was given orally to rats subjected to MTBI. Treatment with a single oral dose of donepezil (12mg/kg) immediately after injury significantly attenuated MTBI-induced neuronal death and cognitive impairment as measured by preservation of neurons in the CA1 region of the hippocampus and a water maze test respectively. However, these neuroprotective effects were prevented by concomitant injection of mecamylamine, a nicotinic acetylcholine-receptor (nAChR) antagonist, indicating that protection is mediated by nAChR activation.

Reduced short latency afferent inhibition in diffuse axonal injury patients with memory impairment.

The present study used short interval intracortical inhibition (SICI), intracortical facilitation (ICF), and short latency afferent inhibition (SAI) to evaluate motor cortex excitability in 16 diffuse axonal injury (DAI) patients with memory impairment and compared the data with those of 16 healthy controls. SAI was reduced in patients compared with controls (92+/-12 versus 39+/-11% of the test size; p<0.0001, unpaired t-test). DAI patients tended to have a high resting motor threshold (RMT) and less pronounced SICI and ICF than controls, but these differences were not significant. A single oral dose (3mg) of donepezil, an acetylcholinesterase inhibitor that is commonly used to treat Alzheimer's disease (AD), improved SAI in DAI patients with wide individual variations that ranged from an increase of 77-18% of test size. These findings suggest that measuring SAI may provide a means of probing the integrity of cholinergic networks in an injured human brain.

Role of protein kinase C in neuroprotective effect of geranylgeranylacetone, a noninvasive inducing agent of heat shock protein, on delayed neuronal death caused by transient ischemia in rats.

We evaluated the neuroprotective effect of geranylgeranylacetone (GGA), an antiulcer agent and inducing agent of heat-shock protein (HSP), against the delayed death of hippocampal neurons induced by transient bilateral occlusion of the common carotid artery (CCA) and hypotension (40 mm Hg) lasting for 10 min. To test the hypothesis that orally administered GGA would induce protein kinase C (PKC), leading to the expression of HSP70 and protection against delayed neuronal death (DND), we gave GGA orally to rats in various regimens prior to bilateral occlusion of the CCA, and quantitatively assessed the extent of DND in region CA1 of the hippocampus at 7 days after transient ischemia. Pretreatment with a single oral dose of GGA of 800 mg/kg at 48 h before ischemia significantly attenuated DND (20.0 +/- 3.81 vs. 321.0 +/- 11.01 mm(3); p < 0.05). A similar degree of neuron sparing occurred when GGA was given 2, 4, or 8 days before ischemia. These neuroprotective effects of GGA were prevented by pretreatment with chelerythrine (CHE), a specific inhibitor of PKC, indicating that PKC may mediate GGA-dependent protection against ischemic DND. Oral GGA-induced expression of HSP70 elicited the expression of PKCdelta, and pretreatment with GGA enhanced the ischemia-induced expression of HSP70, both of which effects were prevented by pretreatment with CHE. These results suggest that a single oral dose of GGA induces the expression of PKCdelta and promotes the expression of HSP70 in the brain, and that GGA plays an important role in neuroprotection against DND. Pretreatment with a single oral dose of GGA provides an important tool for exploring the mechanisms of neuroprotection against DND of hippocampal neurons after transient ischemia.