Case Report
 
Bilateral Peroneal Axonal Neuropathy: A Rare Post-malarial Neurological Syndrome
 

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Nikhil Gupta, Nishant Singh1, Sarthak Malik
From the Department of Medicine, University College of Medical Sciences & GTB Hospital, Dilshad Garden & Maulana Azad Medical College1, Bahadur Shah Zafar Marg, University of Delhi,
Delhi, India.


Corresponding Author
:
Dr. Nikhil Gupta
Email: nik.gupta4u@gmail.com


Abstract

Malaria still remains a leading cause of morbidity and mortality in humans despite intensive efforts from government and sanitary bodies to control malaria. Common presentations of malaria include intermittent fever with chills and rigors, jaundice, renal failure, myalgia etc. In endemic regions, malaria can present with unusual features due to development of immunity, indiscriminate use of antimalarial drugs and increasing resistance to antimalarial drugs. Post malaria neurological syndrome has been described in literature as a rare complication of malaria. To our knowledge, bilateral peroneal axonal neuropathy as a post malaria neurological syndrome is an undescribed entity. We report an unusual and a rare presentation of falciparum malaria.

Introduction

Malaria is a common parasitic infection worldwide affecting 5% of the world’s population at any time [1]. More than two billion people are exposed to Plasmodium falciparum in malaria endemic areas translating into 515 million malaria episodes and more than one million malaria-related deaths each year [2]. Classical presentation is seen in only 50%–70% of the cases with the rest having atypical manifestations. Uncommon presentations are much more common with falciparum species. Various unusual manifestations of falciparum species include hemiplegia, cranial nerve palsies, myelitis-like syndrome, psychosis, cerebellar ataxia, peripheral neuropathy etc. We present to you such an unusual and uncommon presentation of falciparum malaria.

Case Report

A male patient resident of Delhi presented to us with intermittent fever with chills and rigors for 10 days, altered sensorium for 5 days, vomiting for 2 days and yellowish discoloration of eyes and urine for 2 days. There was no history suggestive of seizures, headache, bleeding manifestations or rash over body. The patient was unconscious at presentation with GCS of 6. Patient was febrile, pale, icteric but hemodynamically stable. There was absence of neck rigidity with no focal neurological deficit. Abdominal examination revealed hepatosplenomegaly. Cardiovascular and respiratory examinations were normal.

Patient had haemoglobin of 8.1 gm% (normal: 13-16), TLC 8100/cumm (normal: 4000-11000), platelet count of 1.17 lac/cumm (normal: 1.5–4), DLC P70L23 and ESR was 13 (normal: 0-10). Kidney functions were deranged with blood urea of 90 mg/dL (normal < 20), serum creatinine of 1.1 mg/dL (normal: 0.6-0.9). Liver functions showed total bilirubin to be 6.7 mg/dL (normal < 1-1.5) with direct component of 3.4 mg/dL (normal- 0.1-0.4), AST/ALT to be 102/123 (normal 0-36). Optimal test and peripheral smear were positive for plasmodium falciparum. CSF examination did not reveal any abnormality.

A diagnosis of complicated falciparum malaria was made and patient was given injectable artesunate and clindamycin with supportive measures. After 2 days of treatment our patient recovered completely and became afebrile. After 3 days i.e 5th day of hospital stay patient complained of inability to stand and walk.  There was no complain of backache, bladder or bowel incontinence. Lower limb examination revealed bilateral normal power at hip and knee joint, while bilateral ankle dorsiflexion and eversion revealed power of 0/5. Muscles responsible for inversion of ankle showed normal power while bilateral toe extension was weak with power of 3/5. Bilateral plantars were flexor and all reflexes of the bilateral lower limb were normal. There were decreased sensations of deep and light touch bilaterally over the outer and posterior aspect of leg with rest of the sensory examination being normal. 

MRI spine did not reveal any abnormality. Nerve conduction studies were done which did not record bilaterally any compound motor and sensory potential over the distribution of peroneal nerve. There were normal conduction velocities in both sensory and motor component in bilateral peroneal as well as other nerves. Hence, a diagnosis of bilateral peroneal axonal neuropathy was made. 

Patient was given regular physiotherapy. After a week, patient showed signs of improvement. Patient was advised regular physiotherapy. The patient started recovering motor and sensory functions. After 5 months of neurological illness, patient had regained complete movements at bilateral ankle joint with power of 5/5 in dorsiflexion and eversion at this joint. Patient can now perceive complete sensations of deep and light touch bilaterally over the outer and posterior aspect of leg.

Discussion

Malaria is a common parasitic infection worldwide affecting 5% of the world’s population at any time [1]. More than two billion people are exposed to Plasmodium falciparum in malaria endemic areas translating into 515 million malaria episodes and more than one million malaria-related deaths each year [2].

Falciparum malaria causes multi organ damage in our body [3]. It can lead to neurological involvement, acute renal failure, hepatitis, hypoglycaemia, psychiatric manifestations etc. Various neuropsychiatric manifestations of falciparum malaria have been described which are classified mainly into three groups [4]: i) Sequelae of cerebral malaria e.g. hemiplegia, cranial nerve palsies, myelitis-like syndrome, cerebellar dysfunction and psychosis, ii) Predominant neuropsychiatric signs and symptoms like psychosis, cerebellar ataxia, convulsions, extrapyramidal disorders, etc. without loss of consciousness during acute stage as a presenting illness, iii) As post-malaria neurological syndrome (PMNS), like cerebellar ataxia, psychosis and tremors. 

PMNS is defined as the acute onset confusion, epileptic seizures, or any other neurological or psychiatric sign occurring with a latency of several days to weeks (generally within 2 months) after an episode of successfully treated P. falciparum malaria [5]. Pathogenesis of PMNS is still not known. It is postulated to be immunologically mediated syndrome as some patients respond dramatically to steroids.

These neuropsychiatric manifestations are not common. Various studies have been done to look for the incidence and prevalence of these manifestations. One such study by Kochar et al of 441 patients with cerebral malaria noted the following neurological sequelae in survivors: psychosis (5.06%), cerebellar ataxia (4.72%), hemiplegia (1.68%), extrapyramidal rigidity (EPR) (1.35%) and peripheral neuropathy (1.01%) complications [4]. 

Peripheral nervous system can be involved in the form of Guillian Barre syndrome or acute inflammatory demyelinating polyneuropathy and peripheral neuropathy as mononeuritis multiplex or polyneuropathy. The exact pathogenesis of acute polyneuropathy in falciparum malaria is not known but has been attributed to immune mediated capillary damage, toxic oxygen radicals, tumour necrosis factor, parasitic emboli obstructing the vasa nervorum, neurotoxin release, nutritional and metabolic disturbances [6]. Most of the times, these neurological manifestations disappear after successful treatment of malaria itself with residual symptoms which disappear over the course of time with symptomatic management. 

Our patient was diagnosed as plasmodium falciparum malaria. The patient recovered from febrile episode. After this recovery, the patient developed bilateral peroneal axonal neuropathy. The patient was managed conservatively and physiotherapy was done. Soon, the patient started showing signs of recovery and recovered completely over a span of 5 months. Thus, our patient satisfied the diagnosis of post malarial neurological syndrome.

Conclusion 

Post malarial neurological syndrome is a recognised entity. Bilateral peroneal axonal neuropathy is a rare post malarial neurological syndrome due to complicated Plasmodium falciparum malaria. This syndrome should be readily identified by the physicians. These patients should be managed conservatively and a close follow up is required until recovery.
 
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