Calprotectin levels in the cerebrospinal fluid reflect disease activity in multiple sclerosis.

Calprotectin is produced by activated monocytes and microglia, and cerebrospinal fluid (CSF) levels could be a marker of neuroinflammation. Calprotectin was detectable in CSF from 13.8% of normal controls, compared to 90.5% of patients with neurological infections (p<0.001). In CSF from patients with multiple sclerosis (MS) and clinically isolated demyelinating syndrome, calprotectin was detected in 64.7% within 2 weeks after symptom debut compared to 30.8% between 2 and 4 weeks and 17.0% thereafter (p<0.001). We conclude that CSF calprotectin reflects the disease activity in MS but does not discriminate between MS and other inflammatory or infectious conditions.

[A stiff-legged man with a bizarre gait]. / En mann med stive bein og bisarr gange.

BACKGROUND: Stiff person syndrome (SPS) is a rare neurological disorder characterized by simultaneous contraction of agonistic and antagonistic muscles. SPS can easily be confused with a psychogenic movement disorder, but the frequent finding of autoantibodies against glutamic acid decarboxylase (GAD65), positive response to immunomodulatory treatment and association with other autoimmune diseases strongly suggests an immununological pathogenesis. CASE REPORT: A 43-year-old man was admitted with a three-year history of stiffness and painful spasms in the left leg, causing walking problems and frequent falls. A clinical examination revealed a bizarre gait, pes equinovarus, and simultaneous contraction of agonistic and antagonistic muscles, but no other neurological deficits. Electromyography was normal except for simultaneous contraction of agonistic and antagonistic muscles. Magnetic resonance imaging of the neuraxis and routine examinations of blood and cerebrospinal fluid were normal. A diagnosis of conversion neurosis was considered, but was not supported by positive evidence. The symptoms gradually evolved to affect the back and both legs. Elevated levels of antibodies against GAD65 in serum and cerebrospinal fluid confirmed the diagnosis SPS three and a half years after symptom debut. Both stiffness and muscle cramps responded excellently to diazepam. CONCLUSION: This report calls attention to a rare neurological disease, in which absence of specific neurological deficits may lead to an erroneous diagnosis of a psychogenic disorder.