Efficacy of combination therapy with gabapentin and guanfacine for paroxysmal sympathetic hyperactivity following hypoxic encephalopathy: a case report

Paroxysmal sympathetic hyperactivity (PSH) is a clinical syndrome of episodic sympathetic hyperactivities following severe acquired brain injury. It is characterized by paroxysmal hyperthermia, tachycardia, hypertension, tachypnea, excessive diaphoresis, and specific posturing. Although the persistence of PSH increases the risk of several adverse events and worsens the prognosis, pharmacological treatments for PSH have not yet been clearly established. We report the valuable case of a 60-year-old man who developed PSH following hypoxic encephalopathy, which was effectively treated with a combination therapy of gabapentin and guanfacine. The present case suggests that combination therapy with gabapentin and guanfacine may be a therapeutic option for PSH.

Clinical Correlates of Frontal Intermittent Rhythmic Delta Activity Without Structural Brain Lesion

Frontal intermittent rhythmic delta activity (FIRDA), rhythmic slow wave pattern lasting several seconds over the anterior leads of electroencephalography (EEG), has been reported in a wide variety of clinical conditions. We investigated the clinical significance of FIRDA without structural brain lesions. We reviewed 7689 EEGs between October 2017 and September 2019 at a university hospital. Patients (age >18 years) who were confirmed to have “nonsignificant neuroimaging” were examined. Clinical data were retrospectively collected, and the estimated cause was carefully decided. We found 83 FIRDA among 7689 EEGs (1.08%). After patients with any structural lesion identified on neuroimaging were excluded, 37 FIRDAs were reviewed. There were 20 (51.35%) patients of metabolic encephalopathy. Six patients showed FIRDA due to neurodegenerative disease (16.21%). In addition, we found 6 (16.21%) of neurodegenerative disease and 5 (13.51%) of hypoxic encephalopathy (cardiac arrest). Four (16.21%) patients were related to systemic infection (10.81%), whereas 2 were related to encephalitis (5.40%). We demonstrated several potential etiologies, including metabolic encephalopathy, neurodegenerative disease, hypoxic encephalopathy, and infections, which should be considered in the case of FIRDA without structural brain lesions.

Clinical conundrum: status epilepticus culminating into acute dystonia myoclonus

A 7-year-old child who suffered from symptomatic focal epilepsy as a sequel to perinatal hypoxia used to have frequent seizures. This time she developed prolonged status epilepticus lasting for over 5 hours. She received a treatment in the form of intravenous midazolam and reinitiation of sodium valproate and clobazam that were discontinued previously. Seizures were controlled over a couple of hours, but she remained unresponsive. Later, she developed acute onset dystonia (day 3 post-status epilepticus) and also myoclonic jerks. She presented to us after 3 weeks of onset of these complaints and we considered hypoxic encephalopathy resulting from prolonged status epilepticus or acute encephalitis or non-convulsive status epilepticus. However, acute onset dystonia and periodicity of myoclonic jerks were pointers against it, and on evaluation, she was diagnosed with atypical fulminant subacute sclerosing panencephalitis (SSPE). Knowing the atypical presentations of SSPE is important in planning management and prognostication.

Abstract 285: Analysis of Neurological Prognosis After Cardiac Arrest Patients by Using Cerebral Regional Oxygen Saturation Monitoring

Objective: To clarify the neurological prognosis of post-resuscitation hypoxic encephalopathy patients on the basis of cerebral autoregulation. Methods: We conducted a prospective, observational cohort study of patients admitted to our urban emergency and critical care center in Japan between 2017 and 2019. Cerebral regional oxygen saturation (rSO 2 ) was measured in patients with cardiopulmonary arrest on hospital arrival or return of spontaneous circulation (ROSC) before hospital arrival. Included in the analysis were patients aged ≥16 years who were transported to our hospital. Patients dying within 24 h of hospitalization were excluded. Immediately after arrival, the cerebral rSO 2 sensor was attached to the patient’s forehead and continuous monitoring was started. Continuous monitoring of cerebral rSO 2 and mean arterial pressure (MAP) was conducted until extubation or 96 hours after ROSC. We divided the patients into the good neurological prognosis group (cerebral performance category: CPC 1, 2) and poor neurological prognosis group (CPC 3-5) and compared them. Results: Among the 37 patients with a mean age (± SD) of 68.9 (± 14.8) years, 12 had a good neurological prognosis and 25 had a poor neurological prognosis. In the good neurological cases, we found that the cerebral rSO 2 value showed biphasic changes followed by a long plateau around the lower limit of the normal rSO 2 range from 12 h after ROSC. However, in the poor neurological prognosis cases, we observed that the cerebral rSO 2 value was unstable. In addition, our data showed that the cerebral rSO 2 values in the good neurological prognosis cases remained almost constant even if MAP changed (Figure). Conclusions: We observed the transition of cerebral rSO 2 and its characteristics after resuscitation in cases with good neurological prognosis. Focusing on the cerebral autoregulation may be useful to predict neurological prognosis in post-resuscitation hypoxic encephalopathy.