Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study of eleven patients presenting with neurological complications following acute viral conjunctivitis, mostly haemorrhagic, is reported and the literature reviewed. A Guillain-Barre syndrome-like profile was seen in six patients while the remaining had features of radiculomyelitis. Besides asymmetrical neurological deficits, protein cell reaction and residual muscle wasting, the occurrence of dysautonomias was the striking feature noted in the patients with a Guillain-Barre syndrome-like profile. The dysautonomic features included fatal paroxysmal hypertensive and hypotensive crises in one patient and self limiting tachycardias, episodic profuse sweating, abnormal expiration-inspiration ratio and valsalva ratio in four patients. High antibody titers to EV-70 virus were seen in five patients. A follow up of one and a half year revealed poor neurologic recovery in patients with radiculomyelitis as compared to good functional recovery in others. The importance of early recognition and appropriate treatment of dysautonomias is emphasised. The probable aetiopathogenesis of the neurological complications including dysautonomias is discussed.
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PMID:Neurological complications following acute viral conjunctivitis: a new profile. 375 Mar 88

Guillain-Barre syndrome (GBS) is a common cause of acute peripheral neuropathy and is characterized by hyporeflexia or areflexia. Hyperreflexia has been rarely reported with acute motor axonal neuropathy. A 10-year-old boy presented with asymmetrical weakness of upper and lower limbs and change of voice. Weakness progressed in the hospital with involvement of multiple cranial nerves, preserved deep tendon jerks with extensor plantar, and normal abdominal reflexes. He was treated with IV immunoglobulin and IV methylprednisolone. He was able to walk with support with normal voice at the time of discharge. GBS should be a differential diagnosis in patients with acute quadriparesis even if there are preserved deep tendon reflexes.
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PMID:Guillain-Barre syndrome with hyperreflexia: A variant. 2240 68

SLE (systemic lupus erythematosus) is a multisystem autoimmune disorder of unknown aetiology which can present with myriad clinical presentation. The neurological manifestations of SLE consist of central nervous system (CNS) and peripheral nervous system manifestations (PNS). The CNS manifestations are aseptic meningitis, cerebrovascular accidents (stroke), demyelinating disorders, headache, involuntary movements like chorea, myelopathy, acute confusional states, cognitive dysfunction, mood disorder, seizures, psychosis and cranial nerve palsies.1 The PNS manifestations are Guillain Barre syndrome (GBS), autonomic disorder, mononeuropathy, polyneuropathy and plexopathy.1 Neuropathy in SLE can be clinically classified as mononeuritis multiplex and symmetrical and asymmetrical polyneuropathy. Symmetrical polyneuropathy being the most commonly seen clinical entity amongst the neuropathies in SLE. The neuropathy can be slowly progressive or acute in onset. Electrophysiologically, neuropathy is classified as axonal neuropathy, small fibre neuropathy, demyelinating neuropathy, mixed axonal-demyelinating sensorimotor polyneuropathy and plexopathy. Axonal neuropathy is further divided into sensory, sensorimotor and mononeuritis multiplex. Demyelinating neuropathy can be of two types: acute inflammatory demyelinating polyneuropathy (AIDP) and sensory demyelinating polyneuropathy. Anecdotal case reports also suggest that CIDP can occur as part of SLE neuropathy.2.
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PMID:SLE Neuropathy-Anything New? 2766 98