Acute ischemic stroke is a medical emergency. The initial evaluation of the potential stroke patient often occurs in a high-acuity area. Medical personnel responsible for establishing intravenous access, initiating cardiorespiratory monitoring, performing blood draws, and performing electrocardiography compete for the patient's attention. Additionally, the presence of aphasia or neglect may limit the patient's ability to provide accurate information. The neurological examination should focus on identifying signs of lateralized hemispheric or brainstem dysfunction consistent with stroke. The National Institutes of Health Stroke Scale (NIHSS) is a validated scale that has gained widespread acceptance as a standard clinical assessment tool. The chapter discusses evidence-based ischemic stroke treatment strategies. Determination of stroke mechanism and prompt initiation of secondary stroke preventative strategies such as anti-thrombotic therapy, aggressive risk-factor management, and carotid revascularization in carefully selected patients provide an opportunity to reduce the future burden of stroke.

This chapter reviews the pathology, epidemiology, treatment and management of Intracerebral hemorrhage and subarachnoid hemorrhage (SAH). Hypertensive intracerebral hemorrhages typically occur in territories perfused by deep perforating arteries coming off the basal cerebral arteries. The advent in early use of CT imaging, however, has documented expansion of intracerebral hemorrhage in almost 40% of the cases. The role of surgery for supratentorial hemorrhages has been extensively evaluated in the management of intracerebral hemorrhage, with most of these studies showing no benefit of surgical evacuation of the hematoma. There are approximately 25-30,000 patients a year with SAH. The initial management strategy for the patient after SAH is to stabilize the patient until the cerebral aneurysm can be identified and secured. Interventional procedures may be needed to open constricted cerebral blood vessels if medical maneuvers are insufficient to improve or prevent the onset of neurological deficits due to vasospasm.

Acute seizures and status epilepticus (SE) are common in various types of acute brain injury. The proportion of patients presenting to the emergency department (ED) with new-onset seizures is estimated at 26%. Acute symptomatic seizures are referred to as provoked seizures, situation-related seizures, and reactive seizures. These are seizures that occur in close temporal relationship to a documented brain insult or at the time of an acute systemic insult. Epilepsy is a tendency toward unprovoked recurrent seizures and is the most common reason for seizure occurrences in the hospital. Most seizures that occur in adulthood are focal seizures that arise from disrupted lobar or hemispheric function. SE is the most feared complication for patients with seizures (PWS) because recurrent seizures and SE are more difficult to suppress than single seizures and can be life-threatening, especially when they occur as a primary complication of a neurological or organ system disease.

Neuromuscular diseases include disorders of anterior horn cells, anterior and posterior roots, plexus, peripheral nerves, neuromuscular junctions, and muscles. Detailed history and physical examination most often provide reliable information to localize the neuromuscular disorder. Motor neuron diseases have in common the dysfunction of the superior or inferior motor neuron. Immune myasthenia gravis is caused by autoantibodies interfering with the normal neuromuscular transmission. Most myopathies are slowly progressing diseases involving predominantly proximal muscles. Corticosteroids are the first-line immunosuppressive treatment in most chronic immune-mediated neuromuscular diseases. Neurological disorders may cause respiratory failure by impairing pulmonary ventilation. For normal ventilation to occur, multiple central and peripheral nervous system structures need to be intact. Respiratory management of neuromuscular respiratory failure requires differentiating between slowly developing conditions in which respiratory failure occurs as an exacerbation of a chronic condition, and rapidly progressive diseases.

Disorders of consciousness range from deep coma in a patient with a mass lesion to delirium in a hospitalized elderly patient. Neurohospitalists are often asked to determine the etiology of the patient's altered state and to provide prognostic information and treatment recommendations. This review addresses the common syndromes associated with consciousness disorders, including coma, vegetative and minimally conscious states and syncope. A comatose patient, by definition, has eyes closed with no response to voice or pain and no comprehensible speech or awareness of self and surroundings. Patients typically evolve into a chronic disorder of consciousness, often initially a vegetative state and then potentially into a minimally conscious state. Syncope is a rapid-onset and self-limited loss of consciousness which is typically accompanied by loss of postural tone. Transient global amnesia (TGA) is a clinically defined condition with abrupt onset of anterograde and variable retrograde amnesia lasting up to 24 hours.

Perturbation in the balance of electrolytes can cause both central and peripheral neurological symptoms. Hyponatremia can be the most challenging electrolyte abnormality to correctly diagnose. Regardless of etiology, neurological manifestations are more likely to be present in acute rather than chronic hyponatremia because the rapid decrease in extracellular sodium precipitates intracellular fluid shifts and cellular edema. Calcium stabilizes electrically excitable cell membranes in nerve and muscle tissue and its derangements can have significant neurological sequellae. Like calcium, magnesium has a stabilizing effect on electrically excitable cell membranes. Phosphate homeostasis is closely tied to that of calcium. Hyperphosphatemia can result in symptomatic hypocalcemia and ectopic calcification but it does not generally have neurological manifestations. Phosphate can also be depleted in malnourished patients. Prompt diagnosis and correct management are important to prevent neurological and systemic complications of electrolyte derangements.

The presenting clinical manifestations of a newly detected brain mass can assist the admitting physician in differentiating between tumor and other etiologies. In a patient with imaging features that are highly suggestive of a malignant primary brain tumor, it is reasonable to proceed directly to brain biopsy or craniotomy after a very limited systemic workup. Glioblastomas (GBM) is the most common primary brain tumor with which hospitalists will be involved. The three components of initial, or upfront, treatment for the patient with GBM are maximal safe debulking surgery, involved field irradiation (RT), and chemotherapy. Systemic cancers usually involve the central and peripheral nervous system through direct metastasis or by compression of neural tissue by metastatic disease in adjacent structures. The abundant vasogenic edema that surrounds many brain tumors may be a significant cause of the symptoms such as headache and focal neurological deficits.

This chapter provides a practical guide for clinicians evaluating patients with suspected central nervous system (CNS) infections. Emphasis is placed on common presentations, differential diagnosis, confirmatory testing, initial treatment options, and monitoring response to therapy. Acute bacterial meningitis is characterized by headache, fever, and neck stiffness. Nausea, vomiting, photophobia and seizures are common. Aseptic meningitis is a nonspecific term applied historically to patients with meningitis and negative blood and cerebrospinal cultures. Encephalitis involves brain parenchyma; fever and altered mentation are the predominant presenting symptoms. Brain abscesses are space-occupying CNS lesions which, depending on size and location, may cause focal neurological deficits. Epidural abscess is a neurological emergency. Neurological complications of HIV infection are common and have evolved with introduction of newer therapies. Patients are now living longer with HIV, and CNS pathogens have largely been replaced by HIV-associated cognitive impairment and peripheral neuropathy.

Acute and subacute spinal cord disorders are an important area of hospital medicine given the high risk of devastating neurological complications. This chapter presents the clinical characteristics, diagnosis, differential diagnosis, treatment and prognosis of the following spinal disorders: spinal epidural abscess, transverse myelitis, cauda equina syndrome, spinal cord injury, vascular myelopathies, and neoplastic disorders. Spinal cord trauma can be acutely life-threatening or result in severe chronic disability. Appropriate initial management is crucial to maximizing eventual neurological function. Like cerebral stroke, vascular myelopathy is considered when myelopathic deficits develop abruptly. Spinal epidural abscess results from hematogenous seeding of infection either directly into the epidural space, or to the vertebral body or intervertebral disk with subsequent spread into the epidural space. Cauda equina syndrome (CES) is most commonly due to anatomical compression from a large central disc. Metastases are the most common type of tumor affecting the spine.