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.

Toxic leukoencephalopathy due to transdermal fentanyl overdose.

Children with altered mental status who present to the emergency department have a broad differential diagnosis. We report a case of a 19-month-old girl who presented in coma and who was later found to have a fentanyl patch adhered to her back. She was found to have changes on brain magnetic resonance imaging consistent with a toxic spongiform leukoencephalopathy but had a good neurologic outcome. This case report illustrates the importance of a thorough physical examination in children in coma and a rarely reported magnetic resonance imaging finding that has been seen in opioid intoxication and is usually associated with severe morbidity and mortality.

Differential modulation of withdrawal reflexes by a cannabinoid in the rabbit.

Inhibition of spinal and trigeminal withdrawal reflexes by morphine and by the cannabinoid agonist HU 210 has been studied in anaesthetized and in decerebrated rabbits. In intact, pentobarbitone-anaesthetized animals, the jaw-depressor reflex (JDR) evoked by stimulation of the tongue, and the reflex elicited in the ankle flexor tibialis anterior (TA) by stimulation of the toes were inhibited to the same extent by morphine (1-30 mg kg(-1) i.v. cumulative). In spinalized, anaesthetized rabbits morphine depressed the JDR to the same level as in non-spinal preparations, but the effect of the opioid on the TA reflex was significantly reduced. All effects of morphine were reversed by naloxone (0.25 mg kg(-1), i.v.). In anaesthetised intact animals, HU 210 depressed the JDR at a dose of 100 nmol kg(-1) i.v. cumulative, reduced reflexes evoked in the knee flexor muscle semitendinosus (ST) by stimulation at the toes at a dose of 30 nmol kg(-1) i.v. cumulative, but had no consistent or significant effects on the TA reflex to toe stimulation. The same results were obtained in spinalized, anaesthetised animals. In decerebrated, spinalized rabbits with no anaesthesia, HU 210 (30 nmol kg(-1)) depressed both ST and TA reflexes evoked by toe stimulation. These data reveal that trigeminal and spinal withdrawal reflexes are equally sensitive to morphine provided the spinal cord is intact, suggesting that at least part of the action of systemic morphine is due to activation of descending inhibition. The present results also show for the first time that cannabinoid agonists can inhibit trigeminal withdrawal reflexes. HU 210 had differential effects on the three reflexes studied depending on the presence or absence of anaesthesia. This is the first occasion on which we have found pharmacological distinctions between withdrawal reflexes, and indicates that spinal sensorimotor processing is more heterogeneous than has been suspected previously.

Intrathecal baclofen withdrawal mimicking sepsis.

Baclofen (Lioresal) is a drug of choice to treat spasticity and is increasingly being administered intrathecally via an implantable pump in cases refractory to oral therapy. Emergency physicians will likely treat patients with baclofen withdrawal or overdose as this treatment becomes more widespread. The syndrome of baclofen withdrawal presents with altered mental status, fever, tachycardia, hypertension or hypotension, seizures, and rebound spasticity, and may be fatal if not treated appropriately. Baclofen withdrawal may mimic other diseases including sepsis, meningitis, autonomic dysreflexia, malignant hyperthermia, or neuroleptic malignant syndrome. Treatment consists of supportive care, reinstitution of baclofen, benzodiazepines, and diagnosis and eventual repair of intrathecal pump and catheter malfunction.

[The severest form of CO poisoning (author's transl)]. / Zur schwersten Verlaufsform der CO-Intoxikation

The case histories of four patients with severe cerebral manifestations as a result of CO poisoning are reported. All patients displayed an acute mesencephalic syndrome in the initial stage. One case developed a fatal bulbar syndrome following a transitional phase. Autopsy showed cerebral oedema, in addition to necrotic areas in the basal ganglia and cerebellar haemorrhage. The other 3 patients developed an apallic syndrome with all the typical features and symptoms. Two of these patients died without showing any improvement, displaying not only necroses in the basal ganglia, but also diffuse destruction of the white matter and, in one case, even of the cortex. The third patient recovered. His recovery took a similar course to that of a case of traumatic apallic syndrome and he was subsequently able to take up normal activities. It is concluded from these four cases that secondary brain oedema precedes the development of the most serious form of CO poisoning and is of grave prognostic significance.