A Previously Healthy Adolescent With Acute Encephalopathy and Decorticate Posturing.

A 14-year-old previously healthy female was transferred from a local emergency department after being found unresponsive at home. Parental questioning revealed she had fever and pharyngitis 2 weeks before presentation. Past mental health history was negative, including concern for past or present suicidal ideation/attempts, suspected substance use, or toxic ingestion. In the emergency department, she was orotracheally intubated due to a Glasgow Coma Scale of 3. She was hemodynamically stable and euglycemic. Electrocardiogram showed sinus tachycardia. She underwent a noncontrast head computed tomography that was normal and subsequently underwent a lumbar puncture. She had a seizure and was given a loading dose of diazepam and fosphenytoin that led to cessation of extremity movements. She was subsequently transferred to the PICU for additional evaluation. Initial examination without sedation or analgesia demonstrated dilated and minimally responsive pupils, intermittent decorticate posturing, and bilateral lower extremity rigidity and clonus, consistent with a Glasgow Coma Scale of 5. Serum studies were unremarkable with the exception of mild leukocytosis. Chest radiograph only showed atelectasis. She was empirically started on antibiotics to cover for meningitis pending final cerebral spinal fluid test results. The pediatric neurology team was consulted for EEG monitoring, and the patient was eventually sent for computed tomography angiogram and magnetic resonance angiogram/venogram. We will review diagnostic evaluation and management of an adolescent patient with acute encephalopathy with decorticate posturing of unclear etiology.

A clinical conundrum: unilateral decerebrate rigidity.

A case is described in which, following a motorcycle accident resulting in a closed head injury, a young woman was rendered unconscious. On examination she was found to have unilateral decerebrate rigidity. Further clinical and radiological examination revealed that there was no damage to the limbs, vertebral column, or spinal cord. Readers are expected to be able to make an anatomical diagnosis on the basis of the facts presented.

Intracranial pressure and muscle activity in patients with decerebrate rigidity.

The authors analyse the relationship between the muscle activity during paroxysms of decerebration and the intracranial pressure. These relationships differ, and depend upon the presence or absence of mesencephalic herniation and patency of the perimesencephalic cisterns, as well as on whether the decerebration posturing has been spontaneous or induced by external stimulus. It is suggested that the magnitude of ICP reaction during decerebration is connected with the possibility of compensating the increased intracranial volume and with the strain imposed upon the brain stem at the mesencephalic level. Close correlations between the vegetative variables occuring during spontaneous DR paroxysms suggest a common excitatory neuronal mechanism. In cases when decerebration is provoked by external stimuli the response becomes more complex and not uniform.