Analysis revealed that 12 amino acids (Eg – ornithine, lysine, arginine, glycine, alanine plus citrulline, leucine, tyrosine and phenylalanine) were raised in patients with high CSF proteins while 6 of the amino acids (alanine plus citrulline, 2 amino-butyric acid, leucin, ornithine and lycine) were raised above normal research range in patients who had normal CSF total proteins [13]

Oct 10, 2024 p14ARF

Analysis revealed that 12 amino acids (Eg – ornithine, lysine, arginine, glycine, alanine plus citrulline, leucine, tyrosine and phenylalanine) were raised in patients with high CSF proteins while 6 of the amino acids (alanine plus citrulline, 2 amino-butyric acid, leucin, ornithine and lycine) were raised above normal research range in patients who had normal CSF total proteins [13]. study revealed AIDP variant of Guillain-Barr syndrome. Cerebrospinal fluid analysis done after 2 weeks were normal during both episodes without albuminocytologic dissociation. She was treated with intravenous immunoglobulin resulting in a amazing recovery. Both episodes had a total clinical recovery in three and four months time respectively, rather a faster recovery than usually expected. Conclusion Recurrence of Guillain-Barr syndrome can occur in a subset of patients with H4 Receptor antagonist 1 Guillain-Barr syndrome even after many years of asymptomatic period. Normal cerebrospinal fluid profile does not exclude Guillain-Barr syndrome and may occur in subsequent recurrences of Guillain-Barr syndrome arising the need for further studies to identify the pathophysiology and the possibility of a different subtype of Guillain-Barr syndrome. not performed Extensor digitorum brevis Second episode In 2014, patient readmitted with numbness and progressive ascending weakness of all four limbs for 3 days duration and experienced developed poor cough response, dysphagia and difficulty in breathing during the following Rabbit Polyclonal to GNAT1 2 days. This episode was preceded by an upper respiratory tract contamination two weeks back. There was no similar illness noted in any of her family members. On examination, flaccid quadriparesis with generalized areflexia was noted with a muscle mass power of 1/5 in lower limbs, 2/5 in upper limbs and 2/5 in neck muscles. Weakness progressed to involve bilateral seventh cranial nerves and bulbar muscle mass without ophthalmoplegia. Rest of the neurological examination including sensory system and other organ system examination were normal except for a resting tachycardia of 130 beats/min without any significant blood pressure fluctuations. Respiratory rate was 30 cycles/min with oxygen saturation of 92 % on air flow. Nerve conduction studies done on day 10 of the illness revealed focal segmental demyelinating type sensory and motor neuropathy with prolonged distal motor latency, delayed F-wave and conduction blocks, concluding as AIDP variant of GBS (Table?1). Electromyogram carried out on day 10 of the illness did not show any evidence of denervation but noted fibrillation potentials of positive sharp waves. CSF analysis on day 10 and a repeat study on day 24 showed normal results without cyto-protein dissociation or pleocytosis (Table?2) Full blood count, blood picture, serum electrolytes, erythrocyte sedimentation rate, blood urea and liver enzymes profile were normal. Serology for em Mycoplasma, Campylobacter jejuni /em , cytomegalovirus, Epstein-Barr computer virus, hepatitis B & C and retroviral studies were unfavorable. Autoimmune panel including anti-nuclear factor was normal. Due to the quick progressive nature of weakness and respiratory distress, patient was mechanically ventilated for 12 days. Diagnosis of GBS was made and intravenous immunoglobulin 0.4 g/kg/day was administered for 5 days. In addition, she received physiotherapy to support her recover in motor function of limbs and speech therapy following extubation. She made a good clinical recovery assessed subjectively as well as objectively and was discharged home on day 28 with a muscle mass power of 4/5 and deep tendon reflexes of +1. Table 2 Laboratory findings of Cerebrospinal fluid during the initial presentation in 2002 and recurrence of Guillain-Barr syndrome in 2014 thead th rowspan=”1″ colspan=”1″ Cerebrospinal fluid profile /th th rowspan=”1″ colspan=”1″ 2002 episode: 1 C Day 14 /th th rowspan=”1″ colspan=”1″ 2014 recurrence C Day 10 /th th rowspan=”1″ colspan=”1″ 2014 recurrence C Day 24 /th H4 Receptor antagonist 1 /thead CSF Glucose (mg/dL)867880Proteins H4 Receptor antagonist 1 (g/dL) br / (normal: 15 C 40 g/dL)302026White blood cells/HPF br / (normal: 0 C 5 cells/HPF)242?Neutrophils %—?Lymphocytes %100100100Red blood cells/HPF5-10Random blood glucose tested at the time of lumba puncture (mg/dL)10211094 Open in a separate window CSF study was performed twice during the episode of recurrence (2014) to clarify the persistence of normal CSF findings during the course of the illness On follow-up, patient had normal neurological examination findings and subsequent nerve conduction study after 4 months revealed normal results (Table?1). Conclusions GBS is an acute, immune mediated inflammatory polyradiculo-neuropathy involving the peripheral nervous system. Onset is usually preceded by an antecedent event in two thirds of the patients, usually an upper respiratory tract H4 Receptor antagonist 1 contamination or a diarrheal illness [1C3], where the causative agent is usually assumed to trigger an immune response against the gangliosides and glycolipids distributed along the myelin sheaths and peripheral nervous system. This results in marked inflammation of the peripheral nerves, resulting in demyelination and defective impulse propagation. It is a heterogeneous group of disorders which involves motor, sensory and autonomic nervous systems to varying degrees depending on the sub type; (1) Acute inflammatory demyelinating polyneuropathy, (2) Acute motor axonal neuropathy, (3) Acute motor sensory axonal neuropathy, (4) Miller Fisher syndrome, (5) Acute pan-autonomic neuropathy and (6) Pure sensory GBS. GBS is usually a monophasic illness, with an annual incidence rate of 1 1.2C3.