Chronic subdural hematoma presenting as reversible Parkinson-like symptoms and bladder and bowel dysfunction in a patient with schizophrenia.

Sir,

Subdural hematoma is a collection of blood accumulated in the subdural space. They become encapsulated in the subdural space. Acute subdural hematomas are considered <1 week old and chronic subdural hematomas are more than 1 month old. The variability of mental state is considered as the most important indicator of chronic subdural hematoma.[1] Chronic subdural hematoma in the elderly is known to present with altered mental state, focal neurological signs, headache, falls, seizures, transient neurological deficits, isolated neurological deficits, extrapyramidal syndromes, and ease of falling syndrome.[2] The estimated incidence of chronic subdural hematomas by Fogelholm and Walkimo is 1.72/100,000 per year, with steeply increasing incidence with age, up to 7.35/100,000 per year in the age group of 70–79 years. Advancing age, fall, head injury, anticoagulants, antiplatelet therapy, bleeding diathesis, alcohol, epilepsy, low intracranial pressure, and hemodialysis are identified as risk factors for chronic subdural hematoma in the elderly.[3] Parkinson-like symptoms are a common form of extrapyramidal side effects of antipsychotics.[4] Reversible Parkinson-like symptoms as the acute presenting feature in chronic subdural hematoma were reported in 24 cases.[5] There was one reported case of paraparesis with involvement of the bladder and bowel as the acute presentation of chronic subdural hematoma.[6] Here, we present a case of chronic subdural hematoma presenting as reversible extrapyramidal symptoms and bladder and bowel dysfunction in a patient with schizophrenia who was on antipsychotics, which was not reported earlier.

A 66-year-old patient with a history of schizophrenia came to the routine clinic follow-up with the features of gradual onset rigidity and bradykinesia over 1 month. As he had been poorly compliant with oral medications with frequent relapses leading to multiple admissions, he was started on fluphenazine decanoate depot medication 8 months ago. His mental state was stable with depot medication, and he was not on any antiparkinsonian drugs like trihexyphenidyl as he was free of any extrapyramidal symptoms. There was no evidence of dementia. The last depot injection was given 1 month before the presentation.

He had an indwelling urinary catheter which was inserted by a general practitioner a week ago as he had developed acute urinary retention. Further inquiry revealed that he had not passed stools for the last 4 days. He had no significant past medical or surgical history.

He was afebrile with normal hemodynamic status. Bilateral upper and lower limbs showed marked increased rigidity with normal power and deep tendon reflexes. There was no extensor planter response. Cranial nerve examination was normal. There was no localized tenderness in the spine and no demonstrable sensory level. His mental state was stable, and there was no autonomic instability.

With the working diagnosis of antipsychotic-induced extrapyramidal side effects, fluphenazine depot injection was withheld. He was started on a morning dose of 2 mg of benzhexol and surgical referral done for evaluation of urinary retention and constipation. His basic biochemical investigations were normal (white blood cell –9.5 × 103/μl, serum Na+ –136 mmol/l, serum K+ – 4.3 mmol/l, and serum creatinine –78 μmol/l). The next day, he developed vomiting and abdominal pain with distended tender abdomen, leading to a diagnosis of intestinal obstruction. X-ray abdomen showed distended bowel loops, but as ultrasound scan of the abdomen revealed no free fluid in the abdomen, he was managed conservatively. His clinical condition deteriorated on the following day with the Glasgow Coma Score (GCS) of 8/15 (Best motor response- 4, Best verbal response -2, Eye opening response-2). A noncontrast computed tomography brain was obtained, and it revealed right-sided chronic subdural hematoma with significant midline shift [Figure 1]. There was no history of head injury, fall, or chronic alcohol consumption. As he was not having risk factors for spontaneous subdural hematoma such as chronic alcohol use, hypertension, brain vascular malformations, or anticoagulant therapy, the origin of chronic subdural hematoma was uncertain.

Figure 1

Chronic subdural hematoma

Urgent subdural hematoma evacuation was arranged. Following evacuation, the patient recovered remarkably with improving GCS. With 1-week rehabilitation, his bladder and bowel functions returned to normal and Parkinson-like symptoms disappeared. Benzhexol was omitted thereafter.

During the subsequent clinic visit, he was well with no Parkinson-like symptoms with stable mental state. He continued to receive his monthly fluphenazine depot injection.

Considering the reversibility observed following surgical interventions, chronic subdural hematoma should be considered in the differential diagnosis of elderly patients with Parkinson-like symptoms following antipsychotics. Associated neurological deficit should be considered as one part of the big picture rather than separate pathological entities. This suggests that the high index of suspicion remains pivotal in the diagnosis of chronic subdural hematoma in the elderly. It is important to exclude subdural hematoma in elderly patients on antipsychotic medications who are presenting with new-onset Parkinson-like features.

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Conflicts of interest

There are no conflicts of interest.