Acute hydrocephalus following heroin induced leukoencephalopathy

Dear Editor,

Heroin-induced leukoencephalopathy is a rare complication of heroin intoxication, and always presents as hypoxic ischemic leukoencephalopathy with periventricular white matter edema and spongiform leukoencephalopathy in cerebral and cerebellar white matter [1, 2]. Acute hydrocephalus following toxic leukoencephalopathy has been reported in carbon monoxide and methadone intoxication [3, 4]. However, acute hydrocephalus following heroin-induced leukoencephalopathy has not been previously reported.

On 14 April 2011, a 37-year-old man found in a hotel presented to our hospital after 1 day of unconsciousness. The rubbish can in the man’s hotel room contained an empty syringe, and there were several needle holes in his forearm. Physical examination showed neck rigidity. Glasgow score on admission was 7/15 (E = 1/4, V = 3/5, M = 3/6). His personal and family history was negative for diabetes, seizure disorders, alcohol abuse, and vascular risk factors. There was no evidence of carbon monoxide poisoning.

Hematological and biochemical examinations including hepatitis B, C virus and HIV serology were normal except for high levels of blood creatine kinase (847.24 U/L) and myoglobin (193 μg/L). Drug screening in urine showed positive for heroin. Lumbar puncture showed mildly increased intracranial pressure of 200 mmH₂O, and cerebrospinal fluid routine test and biochemistry were negative. A magnetic resonance imaging (MRI) of the brain revealed abnormally low signal intensity in T1-weighted and high signal intensity in T2-weighted images in bilateral cerebellar hemispheres (Fig. 1a). No abnormality was found in the cerebral magnetic resonance angiography. Toxic leukoencephalopathy was suspected.

Fig. 1

Neuroimaging findings. a Two days after hospital admission, an MRI shows high signal intensity in T2-weighted images in bilateral cerebellar hemispheres (arrows). b Five days after hospital admission, an MRI shows an increase in the size of the lesions in the bilateral cerebellar hemispheres with diffuse cerebellar swelling and compression of the fourth ventricle (arrow). c Five days after hospital admission, a DWI shows an high signal intensity in the bilateral cerebellar hemispheres (arrow). d Seven days after hospital admission, a CT shows hypodense lesions in the bilateral cerebellar hemispheres, constriction of the fourth ventricle (upper left arrow), and dilatation of the third (upper right arrow) and lateral ventricles (lower). e Twenty days after hospital admission, a CT shows that the damage to the bilateral cerebellar hemispheres is reduced, and the fourth ventricle (upper left arrow), the third ventricles (upper right arrow), and lateral ventricles (lower) have returned to normal. f Forty-five days after hospital admission, an MRI shows that the lesions to bilateral cerebellar hemispheres are reduced

Mannitol and dexamethasone were administered, and the man became confused on the second day. Surprisingly, a repeat MRI of the brain on the fifth day revealed enlarged lesions in the bilateral cerebellar hemispheres and compression in the fourth ventricle (Fig. 1b), and diffusion weighted image (DWI) showed a high signal intensity in the bilateral cerebellar hemispheres (Fig. 1c). The man fell into a coma accompanied by dyspnea on the seventh day of admission. A computed tomography (CT) of the brain showed hypodense lesions in bilateral cerebellar hemispheres, the fourth ventricle vanishing, and dilatation of the lateral and third ventricles, indicating acute obstructive hydrocephalus (Fig. 1d). Tracheotomy and surgical external drainage of the hydrocephalus were applied, the consciousness and respiration recovered on the twentieth day while the ataxia and pyramidal signs remained. A brain CT showed that the hydrocephalus was improved (Fig. 1e). The man admitted to 1 year of heroin abuse by intranasal and intravenous administration about 1–3 g a day and confirmed that he had injected an extensive quantity of heroin on the day of onset. This pattern confirmed the diagnosis of acute heroin intoxication accompanied with leukoencephalopathy and acute hydrocephalus. Following a month of treatment, his symptoms were resolved and the imaged lesions were absorbed (Fig. 1f).

To the best of our knowledge, this report is the first description of acute hydrocephalus in heroin-induced leukoencephalopathy. The specific mechanism of delayed neurological deterioration after acute intoxication is unclear. It is usually attributed to cerebellar edema resulting from acidosis, hypoxemia, and toxic effects [3, 4]. Although acute hydrocephalus is not a common complication of acute heroin intoxication, it can occur when recurrent neurological deterioration following from heroin overdose. Imaging is beneficial for early diagnosis and evaluation of progression. Once acute hydrocephalus is confirmed, dehydrants or even surgery is recommended to relieve the cerebral edema and intracranial hypertension. The good prognosis of our patient indicates that heroin-induced leukoencephalopathy and secondary acute hydrocephalus are reversible in some condition. Timely and effective intervention was critical to achieve the best prognosis.