Aggravation of brainstem symptoms caused by a large superior cerebellar artery aneurysm after embolization by Guglielmi detachable coils--case report. (1/22)

An 81-year-old male presented with right oculomotor nerve paresis and left hemiparesis caused by a mass effect of a large superior cerebellar artery aneurysm. Endovascular treatment was performed using Guglielmi detachable coils. The patient subsequently suffered aggravation of the mass effect 3 weeks after the embolization. Bilateral vertebral artery occlusion was performed, which decreased the cerebral edema surrounding the aneurysm, but his neurological symptoms did not improve. Parent artery occlusion is recommended as the first choice of treatment for an unclippable large or giant aneurysm causing a mass effect on the brainstem.  (+info)

Residual cerebral activity and behavioural fragments can remain in the persistently vegetative brain. (2/22)

This report identifies evidence of partially functional cerebral regions in catastrophically injured brains. To study five patients in a persistent vegetative state (PVS) with different behavioural features, we employed [(18)F]fluorodeoxyglucose-positron emission tomography (FDG-PET), MRI and magnetoencephalographic (MEG) responses to sensory stimulation. Each patient's brain expressed a unique metabolic pattern. In three of the five patients, co-registered PET/MRI correlate islands of relatively preserved brain metabolism with isolated fragments of behaviour. Two patients had suffered anoxic injuries and demonstrated marked decreases in overall cerebral metabolism to 30-40% of normal. Two other patients with non-anoxic, multifocal brain injuries demonstrated several isolated brain regions with relatively higher metabolic rates, that ranged up to 50-80% of normal. Nevertheless, their global metabolic rates remained <50% of normal. MEG recordings from three PVS patients provide clear evidence for the absence, abnormality or reduction of evoked responses. Despite major abnormalities, however, these data also provide evidence for localized residual activity at the cortical level. Each patient partially preserved restricted sensory representations, as evidenced by slow evoked magnetic fields and gamma band activity. In two patients, these activations correlate with isolated behavioural patterns and metabolic activity. Remaining active regions identified in the three PVS patients with behavioural fragments appear to consist of segregated corticothalamic networks that retain connectivity and partial functional integrity. A single patient who suffered severe injury to the tegmental mesencephalon and paramedian thalamus showed widely preserved cortical metabolism, and a global average metabolic rate of 65% of normal. The relatively high preservation of cortical metabolism in this patient defines the first functional correlate of clinical- pathological reports associating permanent unconsciousness with structural damage to these regions. The specific patterns of preserved metabolic activity identified in these patients do not appear to represent random survivals of a few neuronal islands; rather they reflect novel evidence of the modular nature of individual functional networks that underlie conscious brain function. The variations in cerebral metabolism in chronic PVS patients indicate that some cerebral regions can retain partial function in catastrophically injured brains.  (+info)

Posterior encephalopathy subsequent to cyclosporin A presenting as irreversible abulia. (3/22)

A case of cyclosporin A (Cys A)-induced posterior encephalopathy developed into persistent abulia despite rapid and marked improvement of abnormal T2- and FLAIR MRI hyperintense regions. Diffusion-weighted MRI signal intensity was also high at the onset. This change is atypical in Cys A-induced encephalopathy and was thought to predict poor recovery from the encephalopathy. Persistent abulia was probably due to marked hypoperfusion in the whole cortex including bilateral frontal lobes and basal ganglia as detected by SPECT. Apart from the breakdown of the blood-brain barrier, direct toxicity of Cys A to the brain may play a role in the pathogenesis of chronic, irreversible encephalopathy.  (+info)

Leukoencephalopathy induced by tegafur: serial studies of somatosensory evoked potentials and cerebrospinal fluid. (4/22)

A case of leukoencephalopathy induced by tegafur, an antineoplastic derivative of 5-FU, is reported. The patient received 600 mg of tegafur p.o. for 16 days before excision of rectal cancer. After the operation, gait disturbance and mental abnormalities appeared. He became akinetic and mute within a few days following readministration of tegafur. Serial studies of brain CT, somatosensory evoked potentials (SEP) were made, and myelin basic proteins (MBP) in the cerebrospinal fluid were measured. The level of MBP was about twice the normal value and the central conduction time (CCT) of SEP was prolonged at admission. The value of MBP and CCT improved with recovery from akinetic mutism.  (+info)

Abulia following penetrating brain injury during endoscopic sinus surgery with disruption of the anterior cingulate circuit: case report. (5/22)

BACKGROUND: It is common knowledge that the frontal lobes mediate complex human behavior and that damage to these regions can cause executive dysfunction, apathy, disinhibition and personality changes. However, it is less well known that subcortical structures such as the caudate and thalamus are part of functionally segregated fronto-subcortical circuits, that can also alter behavior after injury. CASE PRESENTATION We present a 57 year old woman who suffered penetrating brain injury during endoscopic sinus surgery causing right basal ganglia injury which resulted in an abulic syndrome. CONCLUSION: Abulia does not result solely from cortical injury but can occur after disruption anywhere in the anterior cingulate circuit--in the case of our patient, most prominently at the right caudate.  (+info)

MRI findings from a case of fulminating adult-onset measles encephalitis. (6/22)

We report a rare case of fulminating adult-onset measles encephalitis. A 34-year-old man developed a comatose state after measles eruptions and ultimately akinetic mutism. Titers of anti-measles IgM antibodies were elevated in both serum and cerebrospinal fluid. Brain magnetic resonance imaging (MRI) 3 months after onset revealed widespread hyperintense lesions in the periventricular white matter and marginal hyperintense lesions in the brainstem on fluid-attenuated inversion recovery and diffusion-weighted images. The marginal lesions in the brainstem are similar to subpial demyelinating lesions seen in postinfectious encephalomyelitis. This case of encephalitis may be related to an autoimmune-mediated process triggered by measles infection.  (+info)

Akinetic mutism after right internal watershed infarction. (7/22)

We describe a 72-year-old man who developed akinetic mutism following a cerebrovascular accident involving his right internal watershed area and responded well to dopaminergic agonists. We discuss this rare condition and the unusual unilateral location of the lesion.  (+info)

Akinetic mutism responsive to bromocriptine following subdural hematoma evacuation in a patient with hydrocephalus. (8/22)

An 11-year-old girl with obstructive hydrocephalus developed akinetic mutism after treatment for hydrocephalus due to aqueductal stenosis by ventriculoperitoneal (VP) shunting. Bilateral chronic subdural hematomas developed about 2 months after insertion of the VP shunt and were evacuated. Postoperatively, the patient developed akinetic mutism, but her condition improved after administration of bromocriptine. Absence of abnormalities on dopamine transporter single photon emission computed tomography, lack of clinical response to levodopa treatment, and normal homovanillic acid concentration in the cerebrospinal fluid all indicated normal dopamine production. Pressure on the periventricular monoamine projections in the thalamus and hypothalamus without major dopamine deprivation in the striatum may have been the most important factors in the development of akinetic mutism in this patient.  (+info)

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