Clinical features usually resemble those of other space-occupying lesions (focal signs, seizures in 25%–35% of patients) with most symptoms related to increased intracranial pressure (ICP) (headache, nausea, vomiting, lethargy, and stupor). Fever occurs in only 50% of cases.

A combination of broad-spectrum antimicrobials, management of raised ICP, neurosurgical drainage or excision, and eradication of the primary infectious focus is indicated. If CT shows only cerebritis or abscess less than 2.5 cm and the patient is neurologically stable, antibiotics without surgery may suffice. Neurologic deterioration usually mandates surgery.

Excision or aspiration is performed for abscesses greater than 2.5 cm in diameter. Aspiration has become the procedure of choice because it is equally effective and less invasive than excision. Empiric antibiotics should be given based on the expected etiologic agents, presumed route and source of infection, predisposing factors, and adjusted based on the cultures. When the cause is unknown, the patient should receive a third- or fourth-generation cephalosporin, for example, ceftazidime 2 g IV q 8 hr (or ceftriaxone 2 g IV q 12 hr) or penicillin (PCN) G 5 MU IV q 6 hr, and metronidazole 500 mg IV q 6 hr. For paranasal sinus sources, administer PCN and metronidazole. In treatment of posttraumatic cases, administer nafcillin 2 g IV q 2 hr (or vancomycin 1 g IV q 12 hr, if methicillin-resistant S. aureus is suspected) and a third-generation cephalosporin such as ceftazidime 2 g IV q 8 hr. Treatment should be given for 6 to 8 weeks, often followed by additional 2 to 6 months of oral therapy or until the resolution of neuroimaging findings. Three to 4 weeks may be adequate in patients treated with surgical drainage. In human immunodeficiency virus (HIV)-positive patients, coverage should be added for toxoplasmosis with pyrimethamine plus sulfadiazine or clindamycin. Mucormycosis is treated with amphotericin B. Antiepileptic drugs may be given for up to 3 months. Routine corticosteroid administration is controversial and should be used only when mental status is significantly depressed and substantial mass effect can be demonstrated on imaging, and therapy should be of short duration.

Mortality rates range from 5% to 15%. Poor prognosis is associated with very young or old age; anaerobic pathogens; large, multiple, deep, cerebellar, or multiloculated abscesses; acute clinical presentation with stupor/coma; intraventricular or subarachnoid rupture; concomitant pulmonary infection or sepsis; and specific organisms (i.e., Aspergillus and Pseudomonas species, fungal). Long-term sequelae include cognitive deficits (developmental delay in children), seizures, and focal deficits.

Spinal epidural abscess (SEA) is an uncommon condition with an estimated incidence of 0.2 to 2.0/10,000 hospital admissions and a peak incidence in the sixth and seventh decades of life. Conditions commonly associated with SEA include diabetes mellitus, intravenous drug misuse, chronic renal failure, alcoholism, and cancer.

The majority of SEAs are thought to result from the hematogenous spread of bacteria usually from a cutaneous or mucosal source with spread to the posterior aspect of the spinal canal. Direct spread from an adjacent source is less common and typically presents within the anterior aspect of the canal. The most common causative organisms are Staphylococcus aureus (57%–73%), Mycobacterium tuberculosis (25%), other gram-positive cocci (10%), gram-negative organisms 18%, and anaerobes 2%.

The initial manifestations of SEA are often nonspecific and include fever and malaise. The classical diagnostic triad consists of fever, spinal pain, and neurologic deficits. However, over time, an untreated abscess may progress from focal back pain, to radicular pain, to neurologic deficits (motor weakness, sensory changes, and bladder or bowel dysfunction), and then paralysis. Once paralysis develops, it may quickly become irreversible. Thus urgent intervention may be required if progression of weakness or other neurologic findings are detected.

Surgical decompression and drainage with systemic antibiotic therapy is the treatment of choice. Empirical antimicrobial must be started early and be delivered intravenously in high doses and immediately following the collection of two sets of blood cultures. Appropriate empiric parenteral regimens include: vancomycin (15–20 mg/kg IV every 8–12 hours. Trough levels should be drawn 30 minutes prior to the next dose) for empiric coverage of methicillin resistant Staphylococcus aureus (MRSA) plus either ceftriaxone (2 g IV q 12 hr) or cefepime (2 g IV q 8 hr) or ceftazidime (2 g IV q 8 hr). Treatment should be continued for at least 4 weeks but may be prolonged for 8 weeks or longer if vertebral osteomyelitis is suspected.

Overall prognosis is poor; 5% die due to uncontrolled sepsis or other complications, irreversible paraplegia occurs in 4% to 22%, and residual motor weakness in 37%.

This condition is most frequently observed in patients with hepatic cirrhosis, bronchial asthma, salicylate intoxication, hypoxia, sepsis, pneumonia, and acute anxiety (hyperventilation syndrome). Acute respiratory alkalosis constricts cerebral arterioles and decreases cerebral blood flow. Confusion accompanied by a slow electroencephalogram (EEG) may develop. Symptoms of milder respiratory alkalosis include paresthesias, dizziness, cramps as a result of coexistent tetany, hyperreflexia, and muscle weakness. More severe alkalosis (pH 7.52–7.65) in patients with respiratory insufficiency and hypoxia may result in a symptom complex of hypotension, seizures, asterixis, myoclonus, and coma. Treatment is to correct the underlying cause.

Acute respiratory acidosis is a condition of low pH and high CO₂ concentration, occurring as a result of impairment of the rate of alveolar ventilation. Causes of acute respiratory acidosis include sedative drugs, brainstem injury, neuromuscular disorders, chest injury, airway obstruction, and acute pulmonary disease. Lethargy and confusion occur as the PCO₂ rises above 55 mm Hg. Seizures, stupor, or coma may occur with levels greater than 70 mm Hg. The serum bicarbonate level is either normal or high, depending on how rapidly the respiratory failure developed. Neurologic manifestations resulting from cerebral vasodilation include headache, increased intracranial pressure, and papilledema. Hyperreflexia or hyporeflexia and myoclonus may also occur.

Chronic respiratory acidosis generally occurs in patients with chronic obstructive pulmonary disease (COPD), restrictive lung disease (e.g., severe kyphoscoliosis), or extreme obesity (Pickwickian syndrome). It is most often symptomatic with acute exacerbations of disease. Compensatory polycythemia often results from chronic hypercapnic states. Hypoventilation or Pickwickian syndrome may manifest as excessive daytime somnolence.

Therapy of respiratory acidosis involves ventilatory support and treating the underlying disorder. The possibility of sedative or narcotic drug ingestion must be suspected in otherwise healthy patients who suddenly develop acute respiratory depression.

Metabolic alkalosis may result from either excessive ingestion of base or excessive loss of acid. Causes of hypokalemic metabolic alkalosis include Cushing syndrome, vomiting or gastric drainage, diuretic therapy, and primary aldosteronism. Neurologic manifestations include paresthesias, cramps (due to tetany), muscle weakness (due to associated hypokalemia), and hyporeflexia. Severe metabolic alkalosis produces a blunted, confused state rather than stupor or coma and may result in cardiac arrhythmias and severe compensatory hypoventilation.

Treatment depends on the underlying cause.

Metabolic acidosis occurs when a decrease in plasma bicarbonate level lowers pH. Cardinal features are hyperventilation and, when severe, Kussmaul respirations. In chronic metabolic acidosis, hyperventilation may be difficult to detect on clinical examination. The most common causes of metabolic acidosis sufficient to produce coma and hyperpnea include uremia, diabetes, lactic acidosis, and ingestion of acidic poisons. Ketoacidosis occasionally develops in severe alcoholics after prolonged drinking episodes. In diabetics treated with oral hypoglycemic agents, lactic acidosis and diabetic ketoacidosis must be considered.

The presence of neurologic symptoms depends on various factors, including the type of systemic metabolic defect, whether the fall in systemic pH affects the pH of the brain and cerebrospinal fluid (CSF), the rate at which acidosis develops, and the specific anion causing the metabolic disorder. All forms of metabolic acidosis produce hyperpnea as the first neurologic symptom. Other manifestations include lethargy, drowsiness, confusion, and mild, diffuse skeletal muscle hypertonus. Extensor plantar responses occur at a later stage. Stupor, coma, or seizures generally develop only preterminally. Because metabolic acidosis is a manifestation of a variety of different diseases, the treatment varies depending on the underlying process and on the acuteness and severity of the acidosis.

Acute disseminated encephalomyelitis (ADEM) is a monophasic multifocal demyelinating disorder of the CNS, often following infection or vaccination. ADEM is more frequent in children; however, it may occur at any age. The most frequent preceding infections are flulike illnesses, nonspecific upper respiratory tract infections, and gastroenteritis. Although viral etiologies are most common, it can also follow a bacterial infections and, in rare cases, parasitic infections. Postvaccination ADEM is seen in approximately 10% of cases and is most common after measles, mumps, and rubella.

Initial presentation may include meningoencephalitis, fever, encephalopathy, seizures, headache, and meningismus. Focal motor or sensory deficits, ataxia, cranial neuropathies, or brain stem pathology may also be seen.

A more severe presentation known as acute hemorrhagic encephalomyelitis may develop.

High-dose intravenous steroids are used based on their efficacy in treating MS relapses. The aim of steroid treatment is primarily to reduce the CNS inflammatory reaction and accelerate clinical recovery.

Methylprednisolone 20 to 30 mg/kg/day in children and 1 g/day in adults for 3 to 5 days, followed by oral prednisolone 1 to 2 mg/kg/day for 1 to 2 weeks, with subsequent tapering over 2 to 6 weeks. The exact duration of steroid taper is not known; however, early discontinuation may convey a higher risk of relapse. IVIG and sometimes PLEX are used as a second line treatment in patients who do not respond to steroids.

In children, ADEM has a favorable prognosis in 60% to 80% of cases. Most children have functional recovery, and severe disability is rarely seen. Mortality is ≤ 5%. Adults have a less favorable prognosis compared with children. Functional recovery is the outcome in 45% to 65% of adult patients. Mortality can be as high as 15%.

Acquired immunodeficiency syndrome (AIDS) is caused by the human immunodeficiency virus (HIV), a retrovirus. Neurologic manifestations can occur at any level of the neuraxis at any stage of infection and can be a result of direct HIV infection, HIV-induced immune dysregulation, opportunistic diseases, or pharmacologic therapy for the disease and its complications. Specific syndromes tend to occur more frequently during particular phases of HIV infection (but can appear at almost any point during the course), and virtually all have been described as the initial presenting feature of HIV infection. Coexistent systemic infections are common and should be specifically sought and treated concomitantly. The standard method for diagnosing HIV infection is measurement of antibody by enzyme-linked immunosorbent assay (ELISA) followed by Western blot for confirmation of ELISA-positive samples. Prior to host antibody response (“window period”), HIV antigen tests (e.g., p24 protein antigen) and nucleic acid (RNA, proviral DNA) tests are more sensitive. Rate of disease progression is directly related to HIV RNA levels (viral load).