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New Findings In Neurology

Statin Therapy Inhibits Remyelination in the Central Nervous System

Remyelination of lesions in the central nervous system contributes to neural repair following clinical relapses in multiple sclerosis. Remyelination is initiated by recruitment and differentiation of oligodendrocyte progenitor cells (OPCs) into myelinating oligodendrocytes. Simvastatin, a blood-brain barrier-permeable statin in multiple sclerosis clinical trials, has been shown to impact the in vitro processes that have been implicated in remyelination. Animals were fed a cuprizone-supplemented diet for 6 weeks to induce localized demyelination in the corpus callosum; subsequent return to normal diet for 3 weeks stimulated remyelination. Simvastatin was injected intraperitoneally during the period of coincident demyelination and OPC maturation (weeks 4 to 6), throughout the entire period of OPC responses (weeks 4 to 9), or during the remyelination-only phase (weeks 7 to 9). Simvastatin treatment (weeks 4 to 6) caused a decrease in myelin load and both Olig2(strong) and Nkx2.2(strong) OPC numbers. Simvastatin treatment (weeks 4 to 9 and 7 to 9) caused a decrease in myelin load, which was correlated with a reduction in Nkx2.2(strong) OPCs and an increase in Olig2(strong) cells, suggesting that OPCs were maintained in an immature state (Olig2(strong)/Nkx2.2(weak)). NogoA+ oligodendrocyte numbers were decreased during all simvastatin treatment regimens. Our findings suggest that simvastatin inhibits central nervous system remyelination by blocking progenitor differentiation, indicating the need to monitor effects of systemic immunotherapies that can access the central nervous system on brain tissue-repair processes.

Treatment of neuro-Behçet’s disease: an update

Neurological manifestations of Behçet’s disease (neuro-Behçet’s disease) present in 5-30% of cases. They are classified into parenchymal and nonparenchymal categories. Poor prognostic factors include multifocal involvement, spinal presentations, more than two attacks per year, progressive course and increased cerebrospinal fluid cell count and protein content at the time of neurologic manifestations. For patients with parenchymal neuro-Behçet’s disease without any poor prognostic factor, azathioprine or methotrexate and corticosteroids are recommended as the first-line treatment. For high-risk patients, intravenous cyclophosphamide and corticosteroids are recommended. If these regimens failed, TNF-alpha-blocking drugs, such as infliximab or etanercept, should be added. Alternating IFN-alpha and then chlorambucil or experimental treatments are the last resorts for most refractory patients. Treatment of venous sinus thrombosis is achieved by using anticoagulation and short-term corticosteroids with or without immunosuppressants.

Gabapentin responsive audiovestibular paroxysmia

Trigeminal neuralgia and hemifacial spasm are well-documented vascular compression syndromes involving the 5th and 7th cranial nerves. Drugs that stabilize the irritated nerves and vascular decompression surgery are accepted treatments. By contrast, the diagnosis and treatment of a comparable syndrome involving the 8th cranial nerve is controversial. We describe two patients with brief, spontaneous, recurrent attacks of tinnitus and vertigo that responded to low dose gabapentin and we argue that this clinical presentation represents the prototypical 8th nerve vascular compression syndrome.

Schizencephaly associated with bipolar II disorder

A 55-year-old man with congenital hemiparesis of the right side, three episodes of generalised tonic-clonic seizure at 16 years of age, and two episodes of severe depression and two episodes of hypomania in the past, presented with severe depression with psychotic symptoms. Computed tomography of the brain showed a grey matter-lined cerebrospinal fluid-filled cleft in the left cerebral hemisphere, involving the temporoparietal region. He was diagnosed to have bipolar II disorder, and was currently severely depressed with psychotic symptoms and schizencephaly. He improved with sodium valproate 1,000 mg/day, quetiapine 450 mg/day and escitalopram 20 mg/day after three weeks without any emergent side effects, and was maintaining well at three months follow-up. Although uncommon, schizencephaly may be considered as one of the differentials in cases of bipolar disorder along with congenital hemiparesis, mental retardation and/or seizures; and neuroimaging should be done to confirm the diagnosis.

Antiepileptic drugs for the prevention of pediatric migraine

Migraine, according to the criteria of the International Headache Society, occurs in about 5 to 10% of children and adolescents. Pediatric migraine can cause a significant impact on quality of life. As stated by the American Academy of Neurology and Child Neurology Society’s migraine guidelines, situations for prophylaxis consideration include recurring migraines that significantly interfere with daily activities, despite acute therapy; frequent headaches; contraindication, overuse, or failure of acute therapy; adverse reactions to acute therapy; cost of acute and preventive therapies; patient preferences; and presence of uncommon migraine conditions. Preventive therapy may be warranted in as many as 30% of young patients with migraine seen in tertiary headache centers. Headache related disability can be measured by scoring systems such as the Pediatric Migraine Disability Assessment Scale. Numerous medications have been studied to prevent migraines in children, including antihistamines, antidepressants, and antihypertensive agents. However, few high quality clinical trials actually demonstrate efficacy in this population. Recently, many studies dealt with the use of antiepileptic drugs in this indication but there is a paucity of placebo controlled studies. Both topiramate (TPM) and divalproex sodium have been studied in a randomized-controlled study. Only TPM showed efficacy, though, clearly, further controlled trials are needed to confirm these data. Besides unproven efficacy, adverse effects of valproic acid, such as weight gain, somnolence, and alopecia may limit its use. Additional studies are warranted before recommending levetiracetam (LVT), zonisamide (ZNS) and gabapentin (GBP) agents for migraine prophylaxis in children and adolescents.

Fatigue in multiple sclerosis

Fatigue is one of the most common symptoms of multiple sclerosis (MS) and is associated with reduced quality of life. The fatigue syndrome is characterized by uncontrollable apathy, exhaustion, fatigability and lack of energy. The mechanisms underlying fatigue in MS are still poorly understood but studies suggest that immune and neuroendocrine factors may play a causative role in the development of fatigue. The first step in management of MS-related fatigue is identifying and eliminating any secondary causes (adverse effects of drugs, infections, sleep disorders, metabolic diseases). As the fatigue syndrome in patients with MS cannot be evaluated objectively in the routine clinical setting, a number of scales have been developed. The Fatigue Severity Scale is a general scale. Additional scales that have been tested in MS include the Fatigue Impact Scale. Therapy of fatigue syndrome consists of modafinil, amantadine, pemoline and non-pharmacological management.


September 19, 2009 - Posted by | 1

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