Aneurysmal subarachnoid hemorrhage presenting as cardiorespiratory arrest.

Three cases of subarachnoid hemorrhage (SAH) due to ruptured developmental (berry) aneurysm are reported. Two patients presented with cardiac arrest and were successfully resuscitated, but the diagnosis of SAH was delayed and this most likely influenced poor final outcome. The third patient presented with irreversible respiratory arrest. The possible mechanisms responsible for SAH-triggered cardiac arrhythmia and/or respiratory arrest are discussed. Absence of previous cardiac history, persistent headache, focal neurologic findings (especially papilledema or subhyaloid hemorrhages) should warn the clinician of the possibility of SAH and warrant further neurologic investigation.

An unusual degenerative disorder of neurons associated with a novel intranuclear hyaline inclusion (neuronal intranuclear hyaline inclusion disease). A clinicopathological study of a case.

A 21-year-old woman with an unusual, progressive, degenerative neurological disorder is described. The disorder is characterized clinically by behavioral abnormality, peculiar involuntary movements, and ataxia starting in early childhood and subsequent development of dementia, choreoathetosis, rectal and bladder incontinence, bulbar and spinal muscular weakness, pes cavus, kyphoscoliosis, and generalized seizures. The clinical manifestations are correlated, with widespread pathological changes affecting almost all neuronal systems. The pathological changes are discussed in relation to the wide spectrum of "multisystem atrophies." Particular attention is directed to the ubiquitous occurrence of a novel intranuclear, eosinophilic, hyaline inclusion in almost all types of central, peripheral, and autonomic neurons. The ubiquitous neuronal involvement seems to explain the diffuse multiple system degeneration. The pathogenesis of the neuronal inclusions is unknown, but it is speculated that the disorder may represent a metabolic abnormality affecting the nuclear protein of neurons, rather than a viral infection. The pathological features, consisting of the neuronal intranuclear hyaline inclusions associated with multiple system atrophy, have not hitherto been described, and "neuronal intranuclear hyaline inclusion disease" is proposed as a name for the disorder. Rectal biopsy demonstrating the intranuclear hyaline inclusions in ganglion cells of the hyenteric plexuses may serve as a diagnostic procedure for the disorder.

Treatment of acute ischemic stroke. Open trial with continuous intravenous heparinization.

To determine safety of early anticoagulation in patients with acute ischemic stroke, 150 consecutive patients were treated with continuous intravenous heparinization for one to 17 days (median, seven days) in an open trial. Fourteen patients had transient ischemic attacks and 136 patients had acute cerebral infarctions (Cls). None of the patients with transient ischemic attacks experienced untoward events. Of those with acute Cl, four patients (3%) suffered a new, or extension of, Cl; six patients (4.4%) suffered hemorrhagic complications, four patients (3%) died during treatment, and six patients (4%) died afterwards. Three of the deaths were related to treatment complications. Only 13 patients (8.6%) experienced fluctuation of deficit. Median hospitalization was 25.5 days. Recovery of function was good to excellent in 81% of the patients with acute Cl; 75% of the survivors were ambulatory, and about 66% of the patients had either a mild or a minimal neurologic deficit at discharge. The incidence of untoward events in patients with acute Cl was high enough (7.4%) for us to conclude that the efficacy of continuous intravenous heparinization in acute ischemic stroke should be established with controlled studies before its routine use can be recommended.

Acute radicular pain as a presenting symptom in multiple sclerosis.

From December 1973 through November 1988, we cared for 11 patients who presented with acute radicular pain and in whom radicular compression was ruled out by imaging techniques. Eventually, multiple sclerosis was diagnosed and judged to be responsible for the acute radiculopathy. The patients (seven women, aged 18 to 40 years; median, 32 years) and four men (aged 23 to 34 years; median, 29 years) were followed up from 6 months to 15 years (mean, 4 years 11 months). They represent 3.9% of 282 newly diagnosed cases of multiple sclerosis during the same 15 years. A retrospective analysis of the characteristics of their illness and its evolution was conducted. Six had lumbosacral radiculopathies; three, cervical and two, thoracic. In six of the 11 patients, symptoms occurred in close relationship to trauma; seven had recurrent radicular pain; four had other pain syndromes; and three others, paroxysmal symptoms. One patient died of complications from multiple sclerosis 3 years after diagnosis. Three others were rated five or greater in the extended Kurtzke disability status scale during follow-up.

Can embolic stroke be diagnosed on the basis of neurologic clinical criteria?

Diagnosis of embolic stroke is based on identification of a source of embolus (SOE) and on neurologic symptoms acknowledged as "clinical criteria." To test the validity of these criteria, we analyzed the symptoms at onset in 193 patients hospitalized after acute cerebral infarction. Patients were grouped according to identification of a cardiac SOE (106 patients), an arterial SOE (38 patients), or no SOE (49 patients). Cross-tabulations demonstrated that only rapidity and loss of consciousness at onset were associated with the presence of a cardiac SOE to a significant degree. Although these symptoms were highly specific for cardiac SOE, they were not sensitive. A distinct clinical neurologic profile from the symptoms and mode of onset was not identified.

Predictors of intracranial pathologic findings in patients who seek emergency care because of headache.

BACKGROUND: Clinical criteria to select patients with headache in whom structural diagnostic studies (computed tomography) have a high yield disclosing intracranial pathologic findings, independent of abnormal findings on neurologic examination, have not been defined. OBJECTIVE: To determine which clinical characteristics predict the presence of intracranial pathologic findings, independently of neurologic examination, in patients with headache. DESIGN: Case-control, consecutive sample. SETTING: Major metropolitan trauma center emergency department. PATIENTS AND MATERIALS: Hospital records of 139 hospitalized and 329 randomly selected patients from 1720 nonhospitalized adult patients, consecutively evaluated for headache in the emergency department, were reviewed. Demographic data, clinical characteristics of the headache, results of neurologic and physical examinations, and diagnostic radiologic and laboratory results were correlated with final diagnosis and outcome at 6 months after emergency department visit. DATA ANALYSIS: Nonparametric statistical analysis. RESULTS: Intracranial pathologic findings were found in 18 (3.8%) of 468 patients. Acute onset and occipitonuchal location of headache, presence of associated symptoms, and patient age of 55 years or older were significantly associated with the finding of intracranial pathology, independently of the findings from neurologic examination. Abnormal findings on neurologic examination alone, whether focal or nonfocal, had a highly significant association and a positive predictive value for intracranial pathology of 39%. CONCLUSIONS: Abnormal results from neurologic examination are the best clinical parameters to predict structural intracranial pathology; however, in patients 55 years or older with headache of acute onset located in the occipitonuchal region that has associated symptoms, computed tomographic scan of the head is justified as part of their clinical evaluation independently of the findings of the neurologic examination.

Antifibrinolytic therapy in subarachnoid hemorrhage caused by ruptured intracranial aneurysm.

There are 25 published studies on the treatment with antifibrinolytic agents of subarachnoid hemorrhage (SAH) caused by ruptured intracranial aneurysm. Twelve of these studies were uncontrolled and, except for one, all reported reduced incidence of rebleeding. Of 13 controlled studies, 9 were randomized, and 3 were also double-blind. In 7, reported decrease in rebleeding was reported, but only 4 showed decreased mortality. Three studies showed no effect, and three reported a higher incidence of rebleeding in treated patients. Discrepancies may be due to the multiple clinical variables of SAH and to flaws in methodology; nevertheless, the data fail to demonstrate that antifibrinolytic therapy alters the natural history of the disease.

Heparin therapy for stroke: hemorrhagic complications and risk factors for intracerebral hemorrhage.

Hemorrhages occurred in 16 (3.1%) of 510 patients treated with continuous intravenous heparin for acute cerebral infarction (269), reversible ischemic neurologic deficit (81), or transient ischemic attack (160). Three patients (0.6%) had intracerebral hematomas. Risk factors included abnormal CT within 24 hours of onset of symptoms (3.2%), severe neurologic deficit (2.8%), two acute infarcts by CT (2.1%), known source of embolus (1.3%), and final diagnosis of cerebral infarction (1.1%). The only identifiable risk factor for systemic hemorrhage (GI 1.0%, GU 0.8%, muscle 0.4%, skin 0.1%) was age over 60 years. The incidence of intraspinal hematoma was 0.6%. Two of the intracerebral hematomas were fatal, and mortality was 31% in patients with hemorrhagic complications; however, the risk of CNS hemorrhage was only 0.8%.

Neurologic status and prognosis after cardiopulmonary arrest: I. A retrospective study.

A retrospective survey of survivors of cardiorespiratory arrest included 34 patients. Twenty-one had a good outcome neurologically and 13 were seriously impaired. Depth and duration of postarrest coma correlated significantly with poor neurologic function. Seventy percent of the seriously impaired patients never regained consciousness and none emerged from coma within 5 days; 90 percent of patients with good outcome were alert within 18 hours after resuscitation. Coma motor unresponsiveness, absent pupillary light reflexes, and absent oculocephalic responses were closely associated with dismal prognosis for neurologic functioning. This retrospective study cannot provide a basis for discontinuation of life support at any specific time.

Cervical myelopathy complicating cerebral angiography. Report of a case and review of the literature.

Transverse cervical myelopathy, at C-6 level, followed injection of Renografin-60 into the right thyrocervical trunk during cerebral angiography. Review of the literature yielded only two cases in which attempted posterior fossa angiography resulted in cervical myelopathy. Two more cases were found. In one, cervical myelopathy occurred during aortography in a patient with coractation of the aorta, and in the other it followed mediastinal angiography. Summation of anoxia, hemorrhage, and cellular toxicity is responsible for spinal cord necrosis following arterial injection of contrast material.

Heparin-induced thrombocytopenia in patients with cerebrovascular ischemic disease.

We studied 137 patients who were treated with heparin for cerebral infarction (73), partially reversible ischemic neurologic deficit (22), or transient ischemic attack (42). Platelet counts were performed before therapy, twice weekly, and at cessation of therapy. Platelets decreased in 118 patients (86%). In 21 (15.3%), platelets dropped greater than or equal to 40%; 9 of 14 new ischemic events and three of six deaths occurred in this group of patients. Because there was a significant association between poor outcome and platelet drop greater than or equal to 40% (p less than 0.001), we believe that platelets should be monitored frequently when patients are treated with heparin for ischemic cerebrovascular disease.

Neurologic prognosis after cardiopulmonary arrest: III. Seizure activity.

Nineteen (30%) of 63 adult survivors of cardiopulmonary arrest had seizures after admission to the hospital. Eleven of 19 had more than one type of seizure. Myoclonic seizures began within 12 hours of the arrest in eight patients, and after 3 or more days in four patients. Only two (17%) patients with myoclonic seizures survived. Partial seizures usually began within 12 hours of the arrest and were controllable with anticonvulsants; 4 of 12 patients survived. Two of four patients with generalized tonic-clonic seizures survived; one of four with "shivering" lived. Overall, patients with seizures had a survival rate of 32% (6 of 19), compared with 43% for patients without seizures. None of the survivors had recurrent seizures within 6 months after hospital admission.

Neurologic prognosis after cardiopulmonary arrest: II. Level of consciousness.

Sixty-three patients with isolated global anoxic-ischemic injury were prospectively evaluated after cardiopulmonary arrest (CPA); 25 (40%) survived, 16 to an excellent recovery, 8 to a good recovery, and 1 with severe deficits. Forty-six percent of the patients achieved full alertness, and only patients who did so survived. Seventy-five percent of patients arousable or initially alert (level of consciousness [LOC] greater than or equal to 4) survived, all but two with excellent outcomes. Twenty-eight percent of patients initially in deep coma (LOC less than or equal to 3) survived, all with excellent or good outcomes. Ninety percent of patients who became fully alert did so within 72 hours. The likelihood of alerting is correlated with the LOC at given intervals after CPA. Reliable predictions of survival and outcome can often be based upon LOC alone within 2 days after CPA.

TIAs: the forewarning of stroke.

TIAs are a neurologic emergency. The risk of cerebral infarction is high and increases with time. You must consider four factors in the patient with TIA: the results of the neurovascular exam, the stroke risk, the patient's general health, and the availability of diagnostic and treatment facilities.

Stroke and the aging of the brain and the arteries.

Stroke continues to be the third most common cause of death and a major cause of disability among those aged 70 years and older. The risk of stroke doubles for every decade after age 55. It is 25% higher in men. Age, cardiovascular disease, and hypertension are major determinants of cerebral blood flow; all have a negative impact on cerebral reperfusion. The risk of stroke can be reduced at any age by treating and correcting concomitant risk factors: hypertension; heart disease and cardiac arrhythmias (treatment with anticoagulants); transient ischemic attacks (treatment by platelet inhibitors or anticoagulants); and carotid stenosis (by endarterectomy). Cessation of smoking, control of diabetes, reduction of serum lipids, and control of obesity can reduce the risk of stroke. When stroke occurs, early treatment with rt-PA and aggressive patient care results in reduced mortality and morbidity and makes for better neurologic outcomes. Finally, prevention of stroke reduces risk of vascular dementia and makes a better functioning advanced age.

Medical treatment of transient ischemic attacks: does it influence mortality?

All randomized studies published on the medical treatment of transient ischemic attacks in which controls received no treatment or placebo and in which mortality was reported were reviewed. Using the odds ratio method, we analyzed the results to determine if treatment had an effect on expected mortality. Studies were analyzed separately according to the treatment modality used. Chronic anticoagulation was used in four studies and platelet inhibitors in 12 (14 trials). This meta-analysis showed that neither treatment modality significantly reduces mortality. Chronic anticoagulation may have an adverse effect, and even though platelet inhibitors appeared to reduce mortality, no significance can be demonstrated, and the 95% confidence intervals did not allow us to rule out the possibility, albeit small, of an adverse effect or no effect at all.

Posterior fossa subdural hematoma demonstrated by vertebral angiography.

A case of spontaneous posterior fossa subdural hematoma secondary to anticoagulation therapy with definitive diagnosis made by vertebral angiography is reported. Vertebral angiographic findings are illustrated and demonstrate primarily mass effect from posterior compartment of posterior fossa and avascular area. Carotid angiography did not show hydrocephalus. A review of the literature was made and this appears to be the first reported case in which a posterior fossa subdural hematoma has been diagnosed by vertebral angiography.