First reported case of dengue presenting as Multifocal motor neuropathy
Dr Rakitha Higgoda at National Hospital of Sri Lanka, Colombo, Sri Lanka and colleagues have reported case of dengue presenting as Multifocal motor neuropathy.The patient had developed multifocal motor neuropathy (MMN) with conduction blocks following dengue infection during the immediate post-infectious period. The present case has been published in the journal BMC Infectious Diseases.
Multifocal motor neuropathy is a rare neurological disorder with an autoimmune aetiology and according to the authors, this is the first reported case of MMN occurring following dengue infection as a post dengue neurological complication.
According to history a 20-year-old Sri Lankan male who was employed as a helper in a grocery admitted in hospital with weakness of both hands of 1 month’s duration. He had been treated for serologically confirmed (Dengue NS1 antigen positive) dengue fever about 5 weeks ago at a local hospital and had fully recovered at that time. He has been given treated as indoor patient for 5 days and the hospital records revealed that he had simple dengue fever with no evidence of fluid leakage.
After Five days of discharge from the hospital he noticed weakness of his right hand when he dropped a glass of water due to poor grip. He felt more weakness in the right hand which was his dominant hand and it was slowly progressive over 1 month. When he came to hospital he could not write or button on his shirt due to the weakness of the hands. His left hand weakness was milder compared to the right. The weakness was confined to hands and did not involve forearms or arms and there was no accompanying numbness, paresthesia or pain.
H also admitted having slight weakness of both feet which did not significantly interfere with walking but there was no associated neck/back pain or bladder/bowel incontinence. There was no complaint of difficulty in breathing, diplopia, dysphagia, nasal regurgitation, dysarthria or fatigability. Also there was no recent history of trauma to the spine/neck or any preceding diarrheal illness or skin rash.
On examination, he had an average built with no pallor, lymphadenopathy or any signs of malnutrition. Also there were no skin rashes or hypopigmented patches although there was minimal small muscle wasting of bilateral hands and feet. No muscle fasciculations were noted. Distal upper limb (hand) power was diminished asymmetrically, right hand demonstrating a power of 3 out of 5 and left hand demonstrating a power of 4 out of 5. All fine finger movements including flexion, extension, abduction, and adduction were affected with some degree of weakness in wrist extension as well. Bilateral supinator and biceps reflexes were diminished.
Distal lower limb (feet) power was also diminished but was less pronounced (power grade 4) when compared to the degree of hand weakness. Bilateral foot dorsiflexion was weak. Ankle jerks were elicited with reinforcement whereas the knee jerks were elicited without reinforcement. There was no objective sensory impairment of touch, pain, temperature, vibration and joint position sensations in both upper and lower limbs. Bilateral plantar responses were down going. No palpable nerve thickening identified. No cerebellar signs were demonstrated and his gait showed a minor degree of high stepping due to weak dorsiflexion. Examination of higher functions and cranial nerves including the fundal examination revealed no abnormality.
On examination his cardiovascular, respiratory systems and the abdomen was essentially normal.
His full blood count revealed white blood cell count: 8.5 × 109/L, platelet count: 274 × 109/L, hemoglobin 12 g/dl with normal red cell indices. Blood picture showed normochromic normocytic cells with some reactive lymphocytes suggestive of a recent viral infection. Serum creatinine 80 μmol/l (60 - 110 μmol/l), serum sodium 138 mmol/l (135 - 145 mmol/l), serum potassium 3.8 mmol/l (3.5 - 5 mmol/l), serum magnesium 0.9 mmol/l (0.8–1.1 mmol/l), serum ionized calcium 1.2 mmol/l (1.05–1.30 mmol/l). Liver profile: AST 21u/l (10 - 40u/l), ALT 13u/l (7–56 u/l), ALP 67u/l (100–360 u/l), serum total bilirubin 0.7 mg/dl (0.1–1.2 mg/dl), serum albumin 36 g/l (35 - 50 g/l), serum globulin 32 g/l (20 - 35 g/l). CPK levels were normal. Inflammatory markers: ESR 25 mm/hour and CRP < 6 mg/dl.
Nerve conduction study revealed findings in keeping with multifocal motor neuropathy with conduction blocks involving the distal upper and lower limb peripheral nerves without any conduction abnormalities in the sensory nerves.
His CSF analysis did not show any increase in proteins or cells and the values were within the normal limits. Anti-GM1 IgM antibody test was not carried out due to the high cost of the test and the patient’s unstable financial background. A sural nerve biopsy (a sensory nerve) was carried out and revealed histologically unremarkable nerve fibres and blood vessels with no evidence of inflammation, atrophy or granulomata formation. A recent dengue infection was confirmed with positive dengue IgM and IgG antibodies with enzyme-linked immunosorbent assay (ELISA).
As the patient fulfilled criteria, the diagnosis of multifocal motor neuropathy with conduction blocks was confirmed. He was then referred to the neurologist and was started on intravenous immunoglobulin (IVIg) therapy (2 g/kg/day) which was given for 5 days. He showed a mild improvement of his neurological weakness with the treatment and outpatient physiotherapy was arranged. The next immunoglobulin dose was planned to be given after 2 weeks.
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