Neurological deficits

With modest impairment of blood flow, this mechanism allows for preservation of oxidative metabolism without alteration in electrical function. However, when CPP and therefore CBF are sufficiently low, OEF reaches a maximum and cannot increase further. Brain tissue ceases to function electrically, resulting in a neurologic deficit. Microvascular collapse occurs, and CBV falls. If the oxygen supply falls low enough, the tissue dies. Of critical clinical importance is the observation that the amount of time it takes for tissue to suffer irreversible damage is inversely related to the severity of the ischemic insult. Tissue that is completely deprived of blood will die within a few minutes, but less severely hypoperfused tissue may survive for many hours, and may be saved by timely thrombolysis that restores perfusion, or perhaps by another therapeutic intervention. 

A significant neurologic deficit expected to result in long-term disability, and attributable to large vessel occlusion (basilar, vertebral, internal carotid, or middle cerebral artery M1 or M2 branches). 

In one study, patients with significant diffusion-perfusion mismatch on MRI, large vessel occlusive disease, and fluctuating neurological deficits were found to be more likely to respond. Induced hypertension correlated with improved cortical cerebral... 

The timing of CEA after ischemic stroke has been a controversial issue. In 1969, the Joint Study of Extracranial Arterial Occlusion reported 42% mortality after CEA in patients with neurological deficits of less than 2 weeks duration, compared with 5% mortality in patients with more than 2 weeks of symptoms. Early evidence also demonstrated an increased risk of intracerebral hemorrhage after early CEA in patients with acute stroke. This led to the conclusion that most complications occurred with early surgical intervention, and resulted in a traditional 4-6 week delay for CEA after an acute stroke. In retrospect, however, there were major problems with patient selection in these earlier reports. Many of the patients... 

For patients who demonstrate continued neurological deterioration despite anticoagulation, local intrathrombus thrombolysis may be beneficial. In case series in which most patients received urokinase, favorable outcome with no major therapeutic morbidity has been described.In one study, 29 patients with angiogram-proven CVST were reviewed retrospectively. Of the 18 who received local urokinase, 17 recovered completely, and 1 was left with a mild neurological deficit. Heparin was given to four patients, three of whom made a complete recovery. Six presented in a comatose state with severe CVST and only supportive measures were used. It is difficult to draw conclusions from these data, as only patients with mild or moderately severe disease were selected for thrombolytic treatment. 

Many clinicians are concerned about the use of DC for dominant hemisphere strokes, but Kastrau et al. found in a retrospective review of 14 dominant hemisphere stroke patients with aphasia that significant improvement (13/14 patients) was achieved in these preselected younger patients who underwent early poststroke DC. In contrast, a retrospective study by Foerch et al. found that older patients fared quite poorly in terms of functional outcome and quality of life, especially in those with severe neurological deficit at admission. These results were replicated by Curry et al., who also found that younger patients also were more likely to require reoperations for continued herniation. Uhl et al. ° found no prognostic value to the side of infarction in their analysis of 188 patients who underwent DC for massive hemispheric infarction. 

The severity of the neurological deficit at the time of stroke onset is a major predictor of stroke outcome. In an analysis of the placebo-treated patients in the National Institute of Neurological Disorders and Stroke (NINDS) recombinant tissue-plasminogen activator (rt-PA) study, the best acute predictor of a poor outcome at 1 year was an National Institute of Health Stroke Scale (NIHSS) score >17 for patients over 70 years. These criteria had a high specificity (98%), but sensitivity was only 31%. The low sensitivity of the acute NIHSS score alone in predicting... 

The proposal that NO or its reactant products mediate toxicity in the brain remains controversial in part because of the use of non-selective agents such as those listed above that block NO formation in neuronal, glial, and vascular compartments. Nevertheless, a major area of research has been into the potential role of NO in neuronal excitotoxicity. Functional deficits following cerebral ischaemia are consistently reduced by blockers of NOS and in mutant mice deficient in NOS activity, infarct volumes were significantly smaller one to three days after cerebral artery occlusion, and the neurological deficits were less than those in normal mice. Changes in blood flow or vascular anatomy did not account for these differences. By contrast, infarct size in the mutant became larger... 

Clinical diagnosis of an acute ischemic word cerebrovascular accident (CVA) causing measurable neurological deficit... 

Ischemic stroke is the abrupt development of a focal neurologic deficit that occurs due to inadequate blood supply to an area of the brain. Most often, this is due to a thrombotic or embolic arterial occlusion leading to cerebral infarction. 

Ischemic stroke is the abrupt development of a focal neurologic deficit that occurs due to inadequate blood supply to an area of the brain. Most often, this is due to a thrombotic or embolic arterial occlusion leading to cerebral infarction. A thrombotic occlusion occurs when a thrombus forms inside an artery in the brain. An embolism refers to a clot originating outside of the brain in which a piece of the clot breaks loose and is carried to the brain. 

It is unknown whether carotid endarterectomy is of value when performed emergently after stroke, meaning within the first 24 hours after symptoms begin.9 It appears that patients with mild to moderate neurologic deficits, crescendo TIAs or stroke-in-evolution can be operated on safely within the first few hours after the onset of symptoms. Patients with more severe neurologic deficits should only be considered for carotid endarterectomy when the procedure can be performed within the first few hours after the onset of symptoms. It is not indicated for patients with permanent deficits from a moderate to severe completed stroke. 

Clinical diagnosis of ischemic stroke causing a measurable neurologic deficit... 

Oral nimodipine is recommended in subarachnoid hemorrhage to prevent delayed cerebral ischemia. Delayed cerebral ischemia occurs 4 to 14 days after the initial aneurysm rupture and is a common cause of neurologic deficits and death. A meta-analysis of 12 studies was conducted and concluded that oral nimodipine 60 mg every 4 hours for 21 days following aneurysmal SAH reduced the risk of a poor outcome and delayed cerebral ischemia.40... 

Neurologic examination Usually, the neurologic physical examination is completely normal. Any neurologic deficits that are identified should be fully investigated, because seizures do not usually cause permanent, detectable neurologic deficits. 

AG, a 20-year-old male college student, is seen by his physician 4 days after an apparent seizure during finals week. According to his roommate, he suddenly fell to the floor and had a generalized tonic-clonic seizure. This seizure lasted for 1 to 2 minutes. The patient was incontinent for urine during the seizure. He was sleepy and confused when the paramedics arrived 1 0 minutes later. Due to final examinations he reports being sleep-deprived. His physical exam is completely normal and no focal neurologic deficits were observed. 

The treatment goals for central nervous system (CNS) infections are to prevent death and residual neurologic deficits,... 

Immunocompromised, history of CNS disease, new onset seizure, papilledema, altered consciousness, or focal neurologic deficit or delay in performance of diagnostic lumbar puncture... 

---