Post-craniectomy intracranial hypotension: potential impact on rehabilitation.

More aggressive neurosurgical management of intractably elevated intracranial pressure has resulted in increased survival of severely brain injured patients, many of whom are transferred for inpatient rehabilitation status post-craniectomy. Positional headache due to intracranial hypotension has been described in the literature, but is rarely reported as a complicating factor for patients receiving rehabilitation therapies. Low cerebrospinal fluid (CSF) pressure symptoms include postural headache, vertigo, nausea, vomiting, visual symptoms, auditory symptoms, and rarely cognitive changes. This report describes a patient who sustained a severe traumatic brain injury requiring craniectomy for management of increased intracranial pressure who subsequently developed intracranial hypotension. One month post-craniectomy, she developed postural headaches with cognitive and functional decline, which significantly impaired her rehabilitation. Aggressive efforts at conservative management including hydration and empiric blood patch were unsuccessful. Once the bone flap was replaced, she made rapid and dramatic functional gains, with total resolution of headache. This paper hypothesizes that the mechanism of low CSF pressure after extensive craniectomy is related to loss of hydrostatic pressure following removal of the skull vault. In rehabilitation of severely brain injured patients with craniectomies, it is important to recognize and appropriately treat this syndrome to avoid compromising patient care and prolonging hospitalization.

Is needle examination always necessary in evaluation of carpal tunnel syndrome?

OBJECTIVE: To investigate whether needle evaluation added any important clinical information to normal nerve conduction studies in the evaluation of carpal tunnel syndromes. DESIGN: Retrospective review of electromyography (EMG) done with the referring diagnosis of possible carpal tunnel syndrome. SETTING: Outpatients seen for EMG evaluation at one university hospital by a single electromyographer. PATIENTS: Consecutive sample of possible carpal tunnel syndrome patients. INTERVENTIONS: None. MAIN OUTCOME MEASURE: We determined whether needle examination was abnormal when nerve conduction studies were normal. RESULTS: In patients in whom only carpal tunnel syndrome was suspected, normal nerve conduction studies predicted that EMG would be normal 89.8% of the time (p = .0494). Testing based on a larger sample size might increase the predictive value. CONCLUSIONS: There may be a subpopulation of patients referred for carpal tunnel syndrome who may be adequately evaluated by nerve conduction studies alone. Additional studies will help evaluate whether this is so.

Prolonged paralysis after treatment with neuromuscular junction blocking agents.

OBJECTIVES: Previous reports have described prolonged paralysis after treatment with neuromuscular junction blocking agents in critically ill patients. The purpose of this study was to further describe a group of patients who developed prolonged weakness after treatment with these agents. DESIGN: Clinical information, electrodiagnostic and muscle pathology results are described in this group of patients. Clinical information includes diagnoses, dosage of neuromuscular junction blocker, other medications affecting the neuromuscular system, and neuromuscular examination and clinical course. SETTING: All patients were seen in the ICUs of three local hospitals. PATIENTS: Included were critically ill patients with a variety of diagnoses, all of whom developed severe weakness after discontinuation of neuromuscular junction blocking agents. INTERVENTIONS: Electrodiagnostic studies and muscle biopsies were performed on several of the patients. MEASUREMENTS AND MAIN RESULTS: All patients had pronounced weakness without sensory loss. Electrodiagnostic and muscle pathology findings were consistent with failed neuromuscular transmission. Although many patients had disorders or were taking medications that can injure the neuromuscular system, no disorder or medication was common to all. Recovery of strength often took several months and most patients were slow to wean from mechanical ventilator support. CONCLUSIONS: Although alternative explanations cannot be excluded with certainty, the use of neuromuscular junction blocking agents may lead to neurogenic atrophy and care must be taken when using them.

Complete hemidiaphragmatic paralysis in a patient with multiple sclerosis.

We present a case history of a patient with definite multiple sclerosis who developed an abrupt onset of unilateral diaphragmatic paralysis, minor increase in lower extremity spasticity and complaint of marked neck stiffness. Her vital capacity during this episode was 600 mL and she was in impending respiratory failure. The diaphragmatic paralysis was demonstrated by radiographic plain films and fluoroscopy. Phrenic nerve stimulation was performed during fluoroscopy and the evoked motor response from the diaphragm recorded. There was a normal amplitude diaphragmatic twitch observed with an evoked motor response latency of 1 ms and amplitude of 300 microV. After high dose intravenous steroids, her neck stiffness and spasticity improved, her vital capacity improved to 1500 mL and her diaphragm regained its normal position and movement confirmed by followup radiographic plain films and fluoroscopy. We postulate the presence of a demyelinating plaque in the brainstem fibers descending to the phrenic nucleus as the etiology of the diaphragmatic paralysis. We are unaware of any other case reports of unilateral "upper motor neuron" phrenic nerve paralysis secondary to multiple sclerosis.