Jeffrey I. Frank

Large hemispheric infarction, deterioration, and intracranial pressure

Neurologic deterioration from large hemispheric infarction with edema (LHIE) often leads to the use of therapies directed at decreasing intracranial pressure (ICP). Many of these ICP therapies can potentially accentuate tissue shifts from unilateral mass lesions and lead to rebound ICP elevations. We sought to determine whether ICP elevation is a common cause of deterioration from LHIE by measuring the initial ICP and cerebral perfusion pressure (CPP) in 19 patients deteriorating to stupor from LHIE within 3 hours of deterioration, after ruling out metabolic aberrations, medication side effects, infection, and seizures and prior to commencement of any ICP-lowering therapies. We evaluated 19 patients aged 23 to 77 years—14 with complete middle cerebral artery and five with complete internal carotid artery territory infarctions. Stupor began 59 ± 37 hours after the stroke onset. ICP monitoring (12 ipsilat-eral Camino, five contralateral ventriculostomy, and two ipsilateral epidural) demonstrated elevation of ICP (>15 mm Hg) in only five patients (26.3%), with group mean initial ICP = 13.4 ± 10 mm Hg. Similarly, the initial CPP was diminished (>55 mm Hg) in only two patients (10.5%), with group mean initial CPP = 74.9 ± 14 mm Hg. Globally elevated ICP is not a common cause of initial neurologic deterioration from LHIE mass effect.

Malignant cerebral edema and intracranial hypertension.

Cerebral edema and intracranial hypertension occur frequently in neurologic patients. Proper understanding of the pathophysiology of each entity allows prompt recognition and rational therapeutic goals, allowing for better neurologic outcome in many disease states. The recognition of cerebral edema as a distinct entity allows the clinician to treat focal pressure gradients in the brain separately from more diffuse intracranial pressure elevations, appreciating the benefits and pitfalls of directed therapies for each process. The treatment of many of the disorders that cause cerebral edema and intracranial hypertension is heuristic, challenging the managing physicians thorough understanding of cerebral hemodynamics and his or her ability to encounter the human aspects of determining appropriate levels of care for individual patients.

Sarcoid peripheral neuropathy

We studied 10 patients with sarcoidosis and peripheral neuropathy. Six had a subacute or chronic axonal sensorimotor neuropathy without cranial neuropathy, beginning months to years after established systemic sarcoidosis. One patient had severe enough diaphragmatic weakness to require mechanical ventilation. Four patients had atypical neuropathies: acute Guillain-Barré syndrome, mononeuritis multiplex, unilateral lumbosacral plexopathy, and a purely sensory neuropathy, all before systemic sarcoidosis became evident, and all except one had cranial nerve abnormalities. Autopsy in one patient with sensorimotor neuropathy showed only scattered foci of lymphocytes in spinal roots and ganglia with nerve fiber loss.

Automatic stepping in the pontomedullary stage of central herniation

Article abstract—Both spontaneous and reflexive movements may occur during the final stages of herniation and following brain death. We describe spontaneous, rhythmic (0.2 to 0.5 Hz), alternating flexion of the hip, knee, and ankle in two patients during the pontomedullary phase of central herniation following a massive hemispheric infarct. Automatic stepping is likely a spinal automatism generated within the spinal locomotion center and regulated by both ascending and descending brainstem tracts. Clinicians and family members of neurologically devastated patients should be aware that this and other movements can occur during the late stages of central herniation preceding and following brain death.

Is in-hospital stroke mortality an accurate measure of quality of care?

We examined the validity of using in-hospital stroke mortality as predicted by the Cleveland Hospital Outcomes Indicators of Care Evaluations(CHOICE) model as a measure of quality of care. A total of 223 patients admitted to the hospital for stroke were evaluated by the CHOICE model, which predicted that 19 stroke deaths would occur. We reviewed the 19 patients with the highest predicted mortality, according to CHOICE, and three additional patients who died following stroke. We found that The CHOICE model accurately predicts in-hospital stroke mortality for large populations but not for individual patients. CHOICE and other stroke outcome models rely heavily on early Do Not Resuscitate orders and coma but exclude important variables found in the literature on stroke. No correlation between in-hospital stroke mortality and quality of care was demonstrated. Mortality prediction models used to guide consumers on where to receive stroke care are potentially misleading, as they do not assess functional neurologic recovery or the process of care that are essential elements of quality.

Vasodepressor carotid sinus syncope associated with a neck mass

We present the hemodynamic and autonomie features of recurrent purely vasodepressor syncope episodes in a patient with left-sided malignant cervical adenopathy involving the carotid sinus. Extreme hypotension lasting 10 to 30 minutes, without change in heart rate, occurred spontaneously and 20 seconds after head-turning. The baseline respiratory sinus arrhythmia, heart rate response to standing and Valsalvas maneuver, and cold-induced blood pressure elevation were normal, indicating normal baroreceptor function between episodes. The episodes abated after 1 week of bedrest but reappeared within 1 day of discharge from the hospital. Syncope no longer occurred after intracranial section of the left glossopharyngeal nerve and upper rootlets of the left vagus. Autonomie testing remained normal postoperatively. A review of the literature indicates that purely vasodepressor syncope has been more common with left carotid sinus lesions.

Management of intracranial hypertension.

Intracranial hypertension is the final common denominator of morbidity and mortality for diverse neurologic problems, and its proper treatment requires the heuristic application of the available therapeutic alternatives when the clinical situation and patients prognosis warrants treatment. The initial therapeutic focus for ICP reduction should be control of factors that may aggravate intracranial hypertension such as inappropriate head and body position, elevated body temperature, pain, noxious stimuli, elevated airway pressure, elevated blood pressure, seizures, and hypotonic intravenous fluids. The appropriate conventional therapies (e.g., hyperventilation, osmotic agents, sedatives, barbiturates, and cerebrospinal fluid removal) should be selected based on the details of each individual case. Surgical removal of intracranial mass lesions may be indicated in some circumstances, particularly for intractable intracranial hypertension and progressive, severe brain tissue shifts.

Prediction of worsening consciousness from edema after hemispheric infarction.

We sought to develop a risk profile that would predict worsening consciousness from edema after hemispheric infarction. Charts were reviewed correlating initial computed tomography scan, neurologic examination, demographic features, and ischemic mechanism with worsening consciousness from massive edema after hemispheric infarction. An edema risk profile composed of two of three clinical factors (gaze preference, hemiplegia, or hemineglect) and evidence of acute cortical infarction on initial computed tomography scan highly correlated with the later development of worsening consciousness from edema. The edema risk profile correlated with worsening consciousness from edema after hemispheric infarction. The profile requires prospective verification before use for family counseling, for anticipatory care, and for randomizing patients in acute stroke trials aimed at controlling the formation and sequelae of edema after ischemic stroke.

An unusual case of postpartum stroke.

Intracranial hemorrhage is a rare peripartum complication. We report a 28-year-old woman, 24 h postpartum, with acute onset of aphasia, right lower facial paresis, and spastic right hemiplegia secondary to hemorrhage into a previously undiagnosed large left parasagittal meningioma. Prompt diagnosis and surgical intervention led to an excellent outcome. Intrameningiomal hemorrhage as a treatable cause of peripartum stroke is discussed.

Respiratory failure with cervicomedullary infarctions

Respiratory failure from brainstem and spinal cord infarction has been described without attention to ventilatory characteristics and prognosis. We describe two patients who suffered from complete aventilation with cervicomedullary infarctions. One achieved full recovery of spontaneous breathing, and the other had persistent aventilation until her death 4 months after her stroke from sepsis. The anatomical extent of the infarction as identified by magnetic resonance imaging was predictive of the recoverability of spontaneous breathing, and important clinical considerations are emphasized when considering weaning a patient from mechanical ventilation after respiratory failure from cervicomedullary infarction.