Blockade of nonselective cation channels is a potential therapeutic approach that has not been attempted in cerebral ischemia, in spite of the ability of these channels to allow cellular calcium influx into neurons. Fenamates are a class of molecules that block these channels, and many congeners are also anti-inflammatory and free radical scavenging. These three mechanisms may contribute to brain damage in ischemia.

Pretreatment or posttreatment with mefenamate (30 mg/kg) was evaluated in a temperature-controlled rat transient focal ischemia model. Quantitative histopathology on 26 coronal sections allowed determination of tissue necrosis and tissue atrophy at one week survival.

Neither pre- nor postischemic administration of a dose previously shown effective in preventing epileptic neuronal necrosis was found to reduce necrosis in cortex, nor in any subcortical structures.

We conclude that nonselective cation channel blockade with mefenamate affords no neuroprotection in this model. Publication bias against negative studies exists in the literature, but we here report negative findings due to the multiple potentially positive actions of the drug. Closer examination of the effects of the molecule, however, reveals several potentially negative effects as well. We conclude there may be inherent weakness in pharmacologic monotherapy, even with molecules having protean potentially beneficial effects. This conclusion seems to have been borne out by the results of recent clinical trials.

Subacute sclerosing panencephalitis (SSPE) is a rare complication of measles virus infection. The disease is characterized by behavioural abnormalities, intellectual deterioration, motor weakness, and generalized myoclonic jerks progressing to coma and death in one to two years in 80% of the cases. The myoclonic jerks are associated with characteristic generalized slow periodic complexes on electroencephalography (EEG). The symptoms and signs of SSPE are frequently quite variable. The clinical course is equally variable and difficult to predict. The characteristic periodic myoclonus can rarely occur unilaterally particularly in the early stages of the disease. As well, the periodic EEG complexes have been reported unilaterally in up to 3% of cases.

A 12-year-old boy, who was seen at a later stage with atypical manifestation of myoclonic body jerks confined entirely unilaterally, combined with contralateral periodic EEG complexes. One could assume clinically that the more diseased hemisphere was responsible for generating the jerks. However, brain magnetic resonance imaging revealed asymmetric hemispheric changes suggesting that the less neurologically damaged hemisphere is responsible for generating the unilateral myoclonic jerks. This has led to the interpretation that the more severely damaged hemisphere has lost the neuronal connectivity required to generate these periodic myoclonic jerks.

Subacute sclerosing panencephalitis may have asymmetric hemispheric involvement, not only early, but also in the advanced stages of the disease, which can result in unilateral periodic myoclonic jerks.

Organophosphate intoxication can cause some well-known life threatening acute neurological complications such as seizures, paralysis, neuromuscular and cardiac conduction disorders. Less often, a predominantly motor and delayed axonal neuropathy can occur. This syndrome is due to inhibition of neuropathy target esterase.

A 30-year-old woman attempted suicide by drinking approximately 1000mg/kg dimethyl-2,2-dichloro vinyl phosphate (DDVP). After a muscarinic and cholinergic syndrome lasting four days, she developed a purely motor distal axonal polyneuropathy on the fifth week after ingestion confirmed by electroneuromyography and sural nerve biopsy. Neurological examination and electroneuromyography revealed a slight recovery at the end of the 21st month.

This case of late onset polyneuropathy caused by organophosphate intoxication had unusual features such as intact sensory nerves and worse prognosis when compared to previously reported cases.

Multiple brain abscesses are serious neurological problems with high mortality and disabling morbidity. The frequency is rising as a result of AIDS and the increasing number of immunocompromised patients.

A 59-year-old woman developed signs and symptoms of diffuse brain dysfunction including fever and neck stiffness. A brain CT scan demonstrated nine contrast-enhancing ring-shaped lesions. Analysis of the cerebrospinal fluid using PCR-technique revealed DNA of Fusobacterium nucleatum. Conservative treatment with antibiotics was successful. The patient recovered with only mild cognitive deficits.

The experience of our patient and the review of the literature indicate that multiple brain abscesses due to Fusobacterium nucleatum are rare. The most probable source is oral infection.

Multiple brain abscesses may be caused by Fusobacterium nucleatum. Cerebrospinal fluid analysis using PCR technique is helpful with diagnosis. Conservative management can be successful.

Among cases of cerebellopontine angle lesions, vascular lesions involving the internal auditory canal are extremely rare. We report a distal fusiform mycotic pseudoaneurysm of the anterior inferior cerebellar artery (AICA) that simulated an acoustic neuroma on presentation.

A 60-year-old woman was investigated for recent onset of acute dizziness. Laboratory and radiographic investigations are presented, as well as the surgical management of the patient and pathological examination of the aneurysm.

An exceptionally rare case of distal mycotic intracanalicular pseudoaneurysm of the AICA with intraluminal thrombus and fusiform anatomy is described. In our review of the literature (1966-present), only five other intracanalicular AICA-aneurysms were encountered, none of which were infectious in etiology. The possible pathophysiologic mechanisms of distal AICA-aneurysms are discussed along with the currently available literature.

Spontaneous tumour regression in small cell lung cancer has previously been suggested in patients with paraneoplastic neurologic syndromes. Rare documentation of this event has occurred in the literature.

The authors report a patient with anti-Hu associated paraneoplastic sensory neuronopathy who had a spontaneous regression of her small cell lung cancer.

This case supports the hypothesis that anti-Hu neurologic syndromes are the consequence of a misdirected immune response to small cell tumours.

The authors present two cases of movement disorders caused by neuroepithelial cysts and highlight their management. Neuroepithelial cysts are ependymal or epithelial lined fluid collections of unknown etiology within the central nervous system parenchyma with no obvious ventricular or subarachnoid connection. Most cysts are asymptomatic, however, some present with seizures, mass effect, or rarely with movement disorders.

The first patient, a 27-year-old female, presented with progressive weakness, dystonic posturing, tremor, ballismus and choreoathetotic movements of her right upper extremity. Her symptoms improved after stereotactic drainage of a neuroepithelial cyst in her basal ganglia but recurred within a year. The second case, a 56-year-old female, presented with diplopia, nystagmus, gait imbalance and hemiparesis. Her symptoms improved after stereotactic drainage of a midbrain neuroepithelial cyst. The cyst reaccumulated over the next few years and she became symptomatic with left arm tremor and facial weakness. Aspiration was again performed with symptomatic improvement for nine months. Her tremor recurred and a cyst access device was placed stereotactically. She improved and has remained stable for over a year.

Simple stereotactic drainage of neuroepithelial cysts has a high recurrence rate. The authors recommend considering placement of a drainage device to facilitate aspiration of the cyst fluid during follow-up, if needed.

Guillain-BarrÈ syndrome (GBS) classically presents with a subacutely evolving areflexic paralysis, with typical laboratory findings of elevated cerebrospinal fluid protein and abnormal nerve conduction studies. There is now an increasing recognition of GBS variants that differ in clinical presentation, prognosis, electrophysiology and presumed pathogenesis. Fulminant cases of GBS have been reported in which a rapid deterioration evolves to a clinical state resembling ìbrain deathî.

A retrospective analysis of two such cases of fulminant neuropathy are described, that includes the clinical course, electrophysiology and neuropathology where available.

We describe two patients that presented with a rapid course of neurological deterioration, lapsing into what resembled a ìclinically brain-deadî state that was subsequently ascribed to a fulminant polyneuropathy. Investigations (electrophysiological, pathological) and the clinical course suggested an axonal neuropathy.

A fulminant neuropathy can result in a clinical state resembling ìbrain deathî through diffuse de-efferentation. Although generally attributed to aggressive demyelination with secondary axonal degeneration, a primary axonopathy can also lead to a similar clinical presentation.

Dural cavernous angiomas are uncommon benign vascular malformations which may present intraoperative difficulties in hemostasis when the diagnosis is not suspected preoperatively. Preoperative diagnosis can be difficult when angiomas show atypical features and share imaging characteristics with other entities.

A patient presented with a radiographically aggressive lesion, subsequently identified as a dural cavernous angioma. The lesion is reviewed and its clinical, radiographic, and pathological features are compared with other vascular malformations.

A 40-year-old man presented with new onset seizures and an enhancing lesion infiltrating the floor of the right middle cranial fossa. Due to its aggressive radiographic appearance, initial considerations included chondrosarcoma, meningioma or metastasis. Pathological examination, however, revealed the lesion to be a cavernous angioma of dura.

This uncommon lesion may present a diagnostic challenge with significant intraoperative implications. T2 sequence hyperintensity in a relevant lesion should raise suspicion of an hemangioma. It is important to be aware of this entity and its potential to mimic other entities on radiographic grounds.

Fusion following anterior cervical discectomy has been implicated in the acceleration of degenerative changes in the adjacent spinal segments. Discectomy followed by implantation of an artificial cervical disc maintains the functionality of the spinal unit, while still providing excellent symptomatic relief. We describe our preliminary experience with implantation of the Bryan Cervical Disc System in two cases of single-level cervical disc herniation.

Two male patients presented with a left C6 radiculopathy, without evidence of myelopathy. Magnetic resonance imaging revealed a disc herniation at C5-6 in both cases. Pre-operative flexion and extension radiographs demonstrated preserved motion at the involved levels.

Following a standard anterior cervical decompression, precision drilling of the vertebral endplates was carried out using a drill attached to a bed-mounted, gravitationally-referenced retraction frame. An artificial cervical disc, composed of a polyurethane nucleus with titanium endplates, was fitted between the contoured endplates without fixation to the vertebral bodies. No complications were experienced during the insertion of the prosthesis, or in the postoperative course. Both patients experienced immediate postoperative resolution of their radicular pain and were discharged from hospital the following day. At nine months following surgery, both patients continue to have complete relief of radicular symptoms. Postoperative radiographs at six months following surgery confirm accurate placement of the prosthesis and preserved mobility of the functional spinal unit.

Insertion of the Bryan artificial cervical disc prosthesis following anterior cervical discectomy is a relatively straightforward procedure, which appears to be safe and provides good clinical results, without requiring additional surgical time. Long-term follow-up is required to assess its safety, efficacy, and ability to prevent adjacent segment degeneration.