A 20 year old Sri Lankan male who was employed as a helper in a grocery, admitted to our unit with weakness of both hands of 1 month’s duration. He was treated for serologically confirmed (Dengue NS1 antigen positive) dengue fever approximately 5 weeks ago at the local hospital and had made an uneventful recovery. He has been given 5 days of inward treatment and the records from the local hospital revealed that he had simple dengue fever with no evidence of fluid leakage.
Five days after discharge from the hospital he has first noticed the weakness of his right hand when he dropped a glass of water due to poor grip. Weakness was more in the right hand which was his dominant hand and it was slowly progressive over 1 month. At the time of presentation to us he could not write or button on his shirt due the weakness of the hands. Weakness of the left hand was milder than that of the right. The weakness was confined to hands and did not involve forearms or arms. He denied any accompanying numbness, parasthesia or pain.
On inquiry he admitted that there was slight weakness of both feet which did not significantly interfere with walking. There was no associated neck/back pain or bladder/bowel incontinence. He did not complain of difficulty in breathing, diplopia, dysphagia, nasal regurgitation, dysarthria or fatigability. He did not give a recent history of trauma to the spine/neck or any preceding diarrheal illness or skin rash.
He had no previously diagnosed long term medical ailments and has not undergone any surgical procedures in the past. He was not on any long term medications and he denied smoking, use of alcohol or illicit drugs. He did not give a family history of any progressive neurological conditions.
On general examination he had an average built with no pallor, lymphadenopathy or any signs of malnutrition. No skin rashes or hypopigmented patches were noted. 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.
Examination of the cardiovascular, respiratory systems and the abdomen was essentially normal.
Investigations revealed the following results
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 (Fig. 1).
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. 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.
