Motor System Interactions in the Beta Band Decrease during Loss of Consciousness.

Communication between brain areas and how they are influenced by changes in consciousness are not fully understood. One hypothesis is that brain areas communicate via oscillatory processes, utilizing network-specific frequency bands, that can be measured with metrics that reflect between-region interactions, such as coherence and phase amplitude coupling (PAC). To evaluate this hypothesis and understand how these interactions are modulated by state changes, we analyzed electrophysiological recordings in humans at different nodes of one well-studied brain network: the basal ganglia-thalamocortical loops of the motor system during loss of consciousness induced by anesthesia. We recorded simultaneous electrocorticography over primary motor cortex (M1) with local field potentials from subcortical motor regions (either basal ganglia or thalamus) in 15 movement disorder patients during anesthesia (propofol) induction as a part of their surgery for deep brain stimulation. We observed reduced coherence and PAC between M1 and the subcortical nuclei, which was specific to the beta band (∼18-24 Hz). The fact that this pattern occurs selectively in beta underscores the importance of this frequency band in the motor system and supports the idea that oscillatory interactions at specific frequencies are related to the capacity for normal brain function and behavior.

Chronic gliosis and behavioral deficits in mice following repetitive mild traumatic brain injury.

OBJECT: With the recent increasing interest in outcomes after repetitive mild traumatic brain injury (rmTBI; e.g., sports concussions), several models of rmTBI have been established. Characterizing these models in terms of behavioral and histopathological outcomes is vital to assess their clinical translatability. The purpose of this study is to provide an in-depth behavioral and histopathological phenotype of a clinically relevant model of rmTBI. METHODS: The authors used a previously published weight-drop model of rmTBI (7 injuries in 9 days) in 2- to 3-month-old mice that produces cognitive deficits without persistent loss of consciousness, seizures, gross structural imaging findings, or microscopic evidence of structural brain damage. Injured and sham-injured (anesthesia only) mice were subjected to a battery of behavioral testing, including tests of balance (rotarod), spatial memory (Morris water maze), anxiety (open field plus maze), and exploratory behavior (hole-board test). After behavioral testing, brains were assessed for histopathological outcomes, including brain volume and microglial and astrocyte immunolabeling. RESULTS: Compared with sham-injured mice, mice subjected to rmTBI showed increased exploratory behavior and had impaired balance and worse spatial memory that persisted up to 3 months after injury. Long-term behavioral deficits were associated with chronic increased astrocytosis and microgliosis but no volume changes. CONCLUSIONS: The authors demonstrate that their rmTBI model results in a characteristic behavioral phenotype that correlates with the clinical syndrome of concussion and repetitive concussion. This model offers a platform from which to study therapeutic interventions for rmTBI.

Endovascular surgery using stents for vertebral artery dissecting aneurysms and a review of the literature.

The treatment of dissecting aneurysms of the vertebral artery (VA) involving the posterior inferior cerebellar artery (PICA) or presenting with hypoplasia of the contralateral VA is controversial. We describe our experience with 4 ruptured and 2 unruptured VA dissecting aneurysms and discuss the efficacy of endovascular surgery using stents. All patients were male; their mean age was 50.7 years. According to World Federation of Neurological Surgeons (WFNS) grading, 3 of the ruptured aneurysms were grade V, the other was grade I. All patients were successfully treated using stents; in 5 we also coil-embolized the aneurysmal lumen. One aneurysm was treated by the placement of 2 stents covering the dissection site; there was a danger of aneurysmal rupture during coil embolization. No technical complications were encountered although one patient suffered minor rebleeding 5 days post-treatment. Delayed vasospasm occurred in 4 cases. According to the Glasgow Outcome Scale (GOS), at 3 months after treatment 2 patients had made a good recovery, one was moderately disabled, one suffered severe disability, and 2 had died. One death each was due to acute myocardial and brain stem infarction. Endovascular surgery using stents may be a useful treatment in patients in poor condition who manifest dissecting VA aneurysms involving the PICA or hypoplasia of the contralateral VA, especially in the acute period after rupture.

Primary central nervous system lymphoma presenting as an acute massive intracerebral hemorrhage: case report with immunohistochemical study.

BACKGROUND: Hemorrhage at presentation in primary CNS lymphoma is extremely rare and only 2 studies have reported it. We experienced a case of hemorrhage in primary CNS lymphoma, but the feature was different from those in the 2 studies mentioned. We report a case of primary CNS lymphoma presenting as an acute massive ICH causing catastrophic mental deterioration, along with immunohistochemical profiles. CASE DESCRIPTION: A 49-year-old woman was admitted with sudden deterioration of mental status. Immediate CT scan showed a massive ICH in the left frontal lobe with perilesional edema and midline shifting. Emergency operation was performed and the hematoma was removed gross totally, including the abnormal lesions distinguished from adjacent normal brain. The histopathologic diagnosis was non-Hodgkin lymphoma, diffuse, large, B cell type with acute hemorrhage, and immunohistochemistry results showed high VEGF immunoreactivity and intermediate CD34 immunoreactivity. CONCLUSION: Primary CNS lymphoma can present as an acute massive ICH, and immunohistochemistry in the present study strengthened the suggestion that VEGF activity is related to the hemorrhage in primary CNS lymphoma.

Spontaneous intracranial hypotension presenting as a reversible dorsal midbrain syndrome.

A 47-year-old woman with postural headache, episodic stupor, and vertical gaze palsy had brain imaging findings consistent with spontaneous intracranial hypotension (SIH), including severe descent of the mesodiencephalic structures and diffuse pachymeningeal enhancement. The source of the cerebrospinal fluid leakage was a ruptured dorsal perineural cyst. Clinical symptoms improved after a targeted epidural blood patch was performed. Dorsal midbrain syndrome has not been reported previously as a manifestation of SIH. Perhaps distortion of structures in this brain region can occur in SIH as it does in obstructive hydrocephalus.

Cerebellar tumour presenting with pathological laughter and gelastic syncope.

There is no report of patients in whom pathological laughter, a rare condition characterized by uncontrollable episodes of laughter usually triggered by unrelated stimuli, was ever closely associated with a loss of consciousness overtly linked with the onset of such uncontrollable laughter, also referred to as a gelastic syncope. A 53-year-old man presented with a 4-month history of syncope following intense and uncoordinated laughter. Physical and neurological examination was normal and the patient had no other typical cerebellar signs. We found a mass in the cerebellar vermis abutting the floor of the fourth ventricle, which upon histological examination after surgery proved to be an ependymoma. We emphasize that pathological laughter and gelastic syncope could represent unique and sole features of a cerebellar disorder.

A 19-year-old male with generalized seizures, unconsciousness and a deviation of gaze.

Light chain deposition disease (LCDD) is a form of monoclonal immunoglobulin deposition diseases (MIDD) which in contrast to light-chain derived (AL) amyloidosis is characterized by non-congophilic, non-fibrillary monoclonal protein deposits. Systemic organ deposits are common with the kidney being a major target organ. A clonal lymphoplasmocytic proliferation, e.g. plasmacytoma, is present in the majority of cases. Here we report on a 19-year-old male who presented with generalized seizures and an enhancing white matter lesion on MRI scans. A stereotactic brain biopsy revealed a low-grade B cell lymphoma with plasmacellular differentiation as well as lambda light chain deposits without birefringence under polarized microscopy. No systemic lymphoma manifestations or systemic light chain deposits were found, nor was a monoclonal gammopathy detectable in serum and urine. After systemic chemotherapy with three courses high-dose methotrexate the size of the lesion and the condition of the patient have remained stable for 24 months now. This is the first description of cerebral LCDD developing without systemic disease in conjunction with the diagnosis of a cerebral low-grade B cell lymphoma. We present the clinical, laboratory and radiological findings and discuss the pathogenesis of this unusual LCDD manifestation.

Giant intrasellar arachnoid cyst manifesting as adrenal insufficiency due to hypothalamic dysfunction--case report--.

A 67-year-old man first noticed loss of pubic and axillary hair in 1992 and then a visual field defect in 2001. He experienced loss of consciousness attributed to hyponatremia in April 2002. Magnetic resonance imaging showed a giant intrasellar cystic mass, 40 mm in diameter, that had compressed the optic chiasm. The patient complained of chronic headache, and neurological examination revealed bitemporal hemianopsia. Preoperative endocrinological examination indicated adrenal insufficiency, and hypothyroidism due to hypothalamic dysfunction. The patient underwent endonasal transsphenoidal surgery. The cyst membrane was opened and serous fluid was drained. Histological examination identified the excised cyst membrane as arachnoid membrane. The patient's headaches resolved postoperatively, but the bitemporal hemianopsia and endocrinological function were unchanged. This arachnoid cyst associated with hypothalamic dysfunction might have been caused by an inflammatory episode in the suprasellar region.

Traumatic axolemmal and cytoskeletal derangement in myelinated axons of human oedematous cerebral cortex and loss of consciousness. An electron microscopic study using cortical biopsies.

Cortical biopsies of 7 patients with clinical diagnosis of severe head trauma and complicated brain trauma with subdural and epidural hematoma, and loss of consciousness were examined with the transmission electron microscope to study axolemmal and cytoskeletal damage in myelinated axons. Granular disintegration of microtubules and misaligned and fragmented neurofilaments, and fragmentation of axolemmal membrane were observed in most patients studied. In some cases a differential response characterized by increased number of neurofilaments and decreased number or disappearance of microtubules was found. In few cases apparently intact microtubules coexisting with fragmented ones were found. These findings are discussed in relation with traumatic brain edema and associated anoxic-ischemic conditions, the Hameroff-Penrose hypothesis relating microtubules and consciousness, and the existing and contemporary knowledge on neural correlates of consciousness.

Klippel-Feil syndrome associated with posterior fossa dermoid cyst. Case report.

A patient with association of Klippel-Feil syndrome and posterior fossa dermoid cyst is presented. The patient, a 36-year-old man, presented with an acute obstructive hydrocephalus due to the cyst and exhibited the typical triad of the Klippel-Feil abnormality with short neck, low hairline implantation and limited neck motion along with a complex cervical vertebrae fusion. The anatomical and clinical features as well as the pathophysiology of this rare association are discussed after a review of the literature.

Reversible delayed leukoencephalopathy following intravenous heroin overdose.

We present serial neuropsychological, magnetic resonance (MR) imaging and EEG changes in a case of widespread CNS myelinopathy due to intravenous heroin overdose complicated by a period of prolonged unconsciousness. Following recovery from the acute overdose, the subject had the delayed onset of akinetic mutism with urinary incontinence. Sequential formal neuro-psychological assessments over 9 months showed evolution from severe global cerebral dysfunction to moderate disturbance of frontal lobe function. Almost complete resolution of diffuse white matter signal changes, accompanied by the development of a degree of volume loss, was evident on serial MR imaging over the same period, and generalized arrhythmic delta-range slowing on the EEG evolved int o a near normal pattern.