The sensitivity of electrodiagnostic criteria in subtype identification at the presentation in patients of Guillain-Barre syndrome

Introduction: Electrophysiology plays a pivotal role in identifying various GBS subtypes. Despite having many electrodiagnostic criteria,studies addressing their applicability in patients of GBS at diagnosis are quite a few. Purpose: This study evaluates the sensitivity of 5 known electrophysiological criteria in patients with GBS at the time of presentation. Material & Methods: Clinical and electrophysiological data of GBS patients admitted with us between January 2011 and December 2016 were collected retrospectively from our hospital database, compiled and analyzed. For each patient, 5 different criteria for the electrophysiological diagnosis of GBS were applied, and the sensitivity of these 5 criteria in the diagnosis was evaluated. Results: A total of 288 patients were included. Closer concordance was noted between the criteria in diagnosing axonal subtype (Range- 36.81% to 41.32%).Italian criteria had the highest sensitivity (41.32%). There was a wider variation in the diagnosis of AIDP (Range- 19.79 to 34.72%). Hadden criteria showed the highest sensitivity (34.72%) closely followed by Ho et al (34.02%). Conclusion: As the timing of Nerve Conduction Studies (NCS) and the severity of disease influence the grouping of each patient into a specific electrophysiologic subtype, one should be cautious in interpreting electrodiagnosticdata. Serial nerve conduction studies may be required to subtype each patient as electrophysiology evolves over the first few weeks of illness.

Botulinum toxin in post-stroke spasticity.

Botulinum toxin therapy is useful in the treatment of post stroke spasticity as seen in many clinical studies. This therapy is always done in conjunction with the physiotherapists. Successful use of botulinum toxin in spasticity requires careful patient and dose selection. Residual function of the spastic limb and the condition of the agonist and antagonist muscles must be carefully assessed. This is to ensure that the overall condition of the patient will improve by inducing partial or complete paralysis of one or more muscles. It is important that the antagonist muscle(s) must have a) sufficiently powerful functional control, or b) be capable of hypertrophy and strengthening if allowed to perform through the appropriate range of motion, or c) be acceptable in the flaccid state. No fixed joint deformity should be present. It is important to check that weakening the spastic limb(s) will not further compromise residual function (including gait). The rationale for the use of botulinum toxin in spasticity is that a velocity-dependant increase in the stretch reflex response in a spastic antagonist muscle may interfere with normal movement in an agonist muscle. However, spasticity may be beneficial in certain situations, eg. leg extension in spasticity may act as a brace in some patients and assist gait. Generally, the side effects associated with botulinum toxin are temporary and well tolerated. The advantages of botulinum toxin are avoidance of anaesthetics, high patient acceptance and persistence of benefit for months. It also facilitates rehabilitation goals, i.e. increased range of motion, ease of hygiene and positioning, and improves quality of life. Its main disadvantage is its high cost.

Post stroke epilepsy.

Stroke is an important cause of acute symptomatic seizures and epilepsy in the elderly. Post stroke early onset seizures occur within two weeks of stroke onset, while late-onset seizures occur after two weeks. The incidence of early seizures is high with lobar hemorrhage, cortical infarcts especially embolic, agitated acute confusional state and increased stroke severity at stroke onset. Both early and late onset post-stroke seizures, left sided cortical infarcts, increased stroke severity and recurrent strokes are the risk factors for post stroke late epilepsy. Post stroke early seizures as well as late epilepsy do not significantly affect long-term outcome and rehabilitation of stroke. Management options for early seizures and late epilepsy vary and need to be individualized.

Pharmacotherapy for secondary prevention of stroke.

Stroke is a leading cause of mortality worldwide. It has well modifiable risk factors, which makes prevention an effective strategy. Antithrombotics and anticoagulants have been the main pharmacological options in secondary prevention. A number of new antiplatelet drugs have been introduced over the past decade. The more recent concepts in the understanding of stroke and atherosclerosis have paved the way for a number of newer pharmacological interventions like angiotensin enzyme inhibitors, statins and vitamins. The pharmacological armamentarium to treat stroke is expanding.

Neuroprotection for acute ischemic stroke : an overview.

The introduction of thrombolytic therapy has not only injected fresh optimism in stroke management, but has also given a fillip to stroke research, and spurred a number of clinical trials in stroke therapy aimed at salvaging potentially viable ischemic brain tissue. Though a large number of neuroprotective drugs are successful in experimental animal models they have not translated to effective clinical therapy due to a variety of reasons. This has led to a lot of introspection on the methodologic issues in stroke trials and also led to better understanding of ischemic brain damage. It may be realistic to expect that the advances in understanding would evolve into effective neuroprotective therapies in the future.

Recurrent Miller fisher syndrome: a case report.

Miller fisher syndrome (MFS) is a variant of Guillain-Barre syndrome characterized by the triad of ophthalmoplegia, ataxia and areflexia. Recurrences are exceptional with MFS. A case with two episodes of MFS within four years is reported. He presented with findings of ophthalmoplegia, ataxia, areflexia, and oropharyngeal weakness and mild distal sensory impairment during both episodes. Electrophysiological findings showed reduced compound muscle action potentials and sensory nerve action potentials with no evidence of conduction blocks. Nerve biopsy showed segmental demyelination. MRI of brain was normal. He responded well to immunoglobulins during both episodes suggesting that immunomodulating drugs have a role in the treatment of MFS.