Neurology India Medknow Publications on behalf of the Neurological Society of India ISSN: 0028-3886 EISSN: 1998-4022 Vol. 59, Num. 5, 2011, pp. 764-766

Neurology India, Vol. 59, No. 5, September-October, 2011, pp. 764-766

Letter to Editor

Encephalopathy as an initial symptom of rhabdomyolysis

Zhaoshi Zheng, Xuemei Han, Ying Chang, Songyan Liu

Department of Neurology, China-Japan Union Hospital, Jilin University, Jilin, China
Correspondence Address: Songyan Liu, Department of Neurology, China-Japan Union Hospital, Jilin University, Jilin, China, yan1966@163.com

Date of Submission: 09-Jul-2011
Date of Decision: 09-Jul-2011
Date of Acceptance: 10-Jul-2011

Code Number: ni11228

PMID: 22019668

DOI: 10.4103/0028-3886.86558

Sir,

A 39-year-old female was admitted for dizziness, vomiting, and delirium of 5 h duration after eating a "special breakfast for keeping fit". There was no history of fever or upper respiratory tract infection. On examination she was in a state of delirium, pupils were 4 mm in size with sluggish reaction to light, there was increase in the muscle tone, and tendon reflexes were brisk. Vitals were: Blood pressure 120/80 mmHg, heart rate 82 beats/min, body temperature 36.8°C, and SpO ₂ 95%. Laboratory tests revealed: Total white blood cell (WBC) count 16.7 × 10 ⁹ with 81% neutrophils, aspartate transaminase (AST) 47U/L, lactate dehydrogenase (LDH) 519U/L, creatinine kinase (CK) 2143 IU/L, MB isoenzyme of creatine kinase (CK-MB) 47.4 IU/L, a-hydroxybutyric acid dehydrogenase (HBDH) 285 IU/L, troponin I 0.00 ng/ml, MB >1000.0 ng/ml, and normal serum ion levels and renal functions. Head computed tomography (CT) scan showed symmetrical effacement of the ventricular system, obliteration of basal cisterns and Sylvian fissure, and cerebral sulci as well as gyral swelling [Figure - 1].

Initially, the patient was managed as a case of infective encephalopathy with anti-edema and other symptomatic measures with MB, CK monitoring. After 20 h of onset of symptoms body temperature was 38.6°C. The next day the level of consciousness improved and she could answer some questions. She complained of whole body weakness. Clinical examination showed: Body temperature 36.7°C, motor weakness of all four limbs (4/5), depressed tendon reflexes, muscle swelling and mild pain with grip. Opening pressure of cerebrospinal fluid (CSF) was 150 mm H ₂ O and CSF analysis was normal. At the time of admission there was progressive increase in serum MB and CK levels [Figure - 2]. The diagnosis was revised as rhabdomyolysis with encephalopathy. Gastrocnemius muscle biopsy showed the loss of muscle straiae and partial degeneration [Figure - 3]. With the diagnosis of rhabdomyolysis, she was well hydrated and forced diuresis with alkalization of urine was instituted with close monitoring of renal functions. With this treatment there was gradual decline of serum MB and CK levels [Figure - 2]. On Day 11 she was fully conscious, muscle power 4+/5, and muscle swelling and muscle pains were much less when compared to the initial evaluation. Serum CK was 244 IU/L and MB was 42 ug/L. At two months follow-up she is asymptomatic with normal motor power.

In rhabdomyolysis there is an extensive necrosis of striated muscle cells and it results due to a variety of causes. In addition to the clinical features, the diagnosis could be considered when serum CK values are more than five times of normal. ^[1],[2] The diagnosis can be further established by muscle biopsy. In our patient the presenting features were those of encephalopathy, which is a rare manifestation in rhabdomyolysis. Diagnosis of rhabdomyolysis was confirmed by elevated serum CK and MB values. Timely institution of treatment in our patient might have averted acute kidney injury. We believe that the neurological symptoms are the non-specific responses to the inflammation caused by rhabdomyolysis. Pathophysiological changes of rhabdomyolysis include accumulation of the tumor necrosis factor-α (TNF-α) in the serum caused by muscle cell necrosis, with massive release of pro-inflammatory cytokines such as interleukin-6 (IL-6), leading to the disruption of endothelial cell function and blood-brain barrier leakage. ^[3],[4] Seven hours after the onset of symptoms the patient showed increased WBC count with neutrophil predominance and at 20 h, body temperature was high. These features are suggestive of systemic inflammatory response to widespread rhabdomyolysis. As part of the systemic inflammatory response the pro-inflammatory cytokines could have acted directly on the tight junction complex between endothelial cells, leading to increased blood-brain barrier permeability and vasogenic brain edema. ^[5] Additionally, IL-β could increase the expression of aquaporin 4 (AQP4), exacerbating the brain edema.^[6] Disturbance in the neurotransmitters including serotonin and dopamine might have also played a role in the pathogenesis of the encephalopathy in this patient. It has been shown that IL-1 or IL-6 cause an increase in the serotonin levels in the cerebrospinal fluid (CSF). ^[7],[8] Moreover, the interleukin, TNF-α and serotonin could also act on the awake system, causing rhythm disorders.^[9],[10]

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