Neuro

When assessing brain function

first address hydration and sleep apnea.

Confusion

Loss of the ability to think rapidly and clearly, impaired judgment and decision making.

Disorientation

Beginning loss of consciousness, disorientation to time, place, and impaired memory.

Lethargy

Limited spontaneous movement or speech, easy arousal with normal speech or touch, may not be oriented to time, place, or person.

Obtundation

Mild-to-moderate reduction in awakeness with limited response to the environment, falls asleep unless stimulated.

Stupor

Condition of deep sleep or unresponsiveness, person may be aroused only by vigorous stimulation.

Coma

No verbal response to the external environment or any stimuli.

Light Coma

Associated with purposeful movement on stimulation.

Deep Coma

Associated with unresponsiveness or no response to any stimulus.

Apneustic respirations

Prolonged inspiratory and expiratory phases caused by injury to the pons or upper medulla.

Cluster respirations

Periods or clusters of rapid respirations resulting from trauma or compression to the medulla or chronic opioid abuse.

Ataxic respirations

Irregular respirations with prolonged periods of apnea associated with damage to the medulla.

Ischemia/hypoxia

Dilated, fixed pupils.

Opiates

Pinpoint pupils.

Brain Death

Body cannot maintain internal homeostasis. Irreversible cessation of the entire brain, including brainstem and cerebellum, occurs.

Brain death criteria

Completion of all appropriate, therapeutic procedures, unresponsive coma, no spontaneous respirations, no brainstem function, isoelectric electroencephalography (EEG) for 6-12 hours.

Cerebral Death/irreversible coma

Death of the cerebral hemispheres, exclusive of the brainstem and cerebellum.

Alterations in awareness

Direct destruction or compression of brain tissue. Indirect destruction as a result of compression. Effects of toxins and chemicals or metabolic derangement.

Agnosia

Failure to recognize the form and nature of objects. Can be tactile, visual, or auditory.

Aphasia

Loss of comprehension or production of language.

Dysphasia

Impaired speech.

Receptive/Wernicke

Disturbance in understanding all language, verbal and reading comprehension.

Conductive

Disruption of temporal lobe fibers with a failure to repeat words but an ability to initiate speech, writing, and reading aloud.

Anomic

Inability to name objects, people, numbers, or qualities.

Transcortical

Ability to repeat and recite.

Expressive/Broca aphasia

Expressive dysphasia of speech and writing but with retention of comprehension.

Global aphasia

Involves anterior and posterior speech areas, with expressive and receptive aphasia.

Acute confusional state

Impaired or lost detection. Fluctuating symptoms. Confusion and restlessness. Inability to focus, maintain attention, or concentrate. Delusions. Hallucinations. Impaired sleep. Dilated pupils.

Treatment of Acute confusional state

Identify the cause, discontinue drugs if necessary, pharmacologic/nonpharmacologic measures, supportive and protective measures.

Delirium

Is an acute state of brain dysfunction. Onset is usually abrupt. Autonomic nervous system is overactive. Is common in critical care units, postsurgically, or during withdrawal from CNS depressants (e.g., alcohol, narcotics). Confusion comes on quickly in days. Hyperkinetic confusional state. Acute state of brain dysfunction. Is associated with the right middle temporal gyrus or disruption of the left temporo-occipital junction.

Hyperactive delirium

Agitated delirium/Excited delirium syndrome.

Hypoactive delirium

Hypoactive confusional state. Is associated with the disruption of the right-sided, frontal-basal ganglion.

Dementia

Is the progressive failure of many cerebral functions. Onset is usually gradual. Progressive dementia produces nerve cell degeneration and brain atrophy. Age is the greatest risk factor.

Alzheimer Disease

Leading cause of dementia, irreversible, characterized by neurofibrillary tangles and neuritic plaques. Specific diagnosis can only be made by postmortem examination.

Frontotemporal Dementia

Rare, severe degenerative disease of the frontal lobes, age of onset is younger than 60 years.

Huntington Disease

Rare, autosomal dominant hereditary-degenerative disorder; short arm on chromosome 4. Severe degeneration of striatum and basal ganglia. Abnormal movements that occur without conscious effort, emotional lability, and dementia.

Parkinson Disease

Severe degeneration of the basal ganglia involving the dopaminergic nigrostriatal pathway.

Parkinson Clinical Manifestations

Wide-eyed, unblinking, staring expression with immobile facial muscles. Frequent drooling. Slow gait. Short, shuffling steps. Flexed and abducted arms held stiffly at the side. Slightly forward bending trunk.

Parkinson Treatment

Drug therapy: levodopa, anticholinergic drugs, antihistamines, amantadine. Surgery. Rehabilitation. Physiotherapy and speech therapy. Occupational therapy, physical therapy, language, and swallowing therapy.

Upper Motor Neuron

Muscle groups are affected. Mild weakness. Minimal disuse muscle atrophy. No fasciculations. Increased muscle stretch reflexes (clasp-knife spasticity; resistance to passive flexion that releases abruptly to allow easy flexion). Clonus may be present. Hypertonia, spasticity. Pathologic reflexes (Babinski and Hoffmann signs, loss of abdominal reflexes). Often initial impairment of only skilled movements.

Lower Motor Neuron

Individual muscles may be affected. Mild weakness. Marked muscle atrophy. Fasciculations. Decreased muscle stretch reflexes. Clonus not present. Hypotonia, flaccidity. Hyporeflexia. No Babinski sign. Asymmetric and may involve one limb only in beginning to become generalized as disease progresses.

ALS

Is a degenerative disorder diffusely involving the lower and upper motor neurons. Movement is more affected than the brain. Progressive muscle weakness leads to respiratory failure. Lower motor neuron syndrome of flaccid paresis consists of a weakness of individual muscles, progressing to paralysis, hypotonia, and primary muscle atrophy (atrophy caused by denervation).Upper motor neuron syndrome of spastic paresis consists of a weakness of movement patterns, progressing to paralysis and atrophy.

ALS Clinical Manifestations

Limb cramping or weakness. Incoordination. Slurring of speech. Difficulty swallowing. Single muscle group. Paresis that spreads. Hypotonia.

ALS Treatment

Administer riluzole (Rilutek), an antiglutamate which is standard treatment that prolongs life for months but does not cure. Maintain quality of life. Involve family in the treatment.

Moderate cerebral concussion

Any loss of consciousness lasting more than 30 minutes, accompanied by posttraumatic anterograde amnesia lasting 24 hours or more.

Postconcussive syndrome

Headache. Nervousness or anxiety. Irritability. Insomnia. Depression. Inability to concentrate, forgetfulness. Fatigability.

Postconcussive syndrome Treatment

Reassurance and symptomatic relief, close observation for 24 hours.

Primary spinal cord injury

Diaphragm function may be impaired because phrenic nerves exit at C3 to C5. Therefore an injury at C4 might impair breathing.

Spinal shock

the complete loss of reflex function in all segments below the level of the lesion. Manifestations include flaccid paralysis, sensory deficit, a disruption in thermal controls (faulty control of sweating), transient drop in BP, and loss of bladder and rectal control. May persist for as short a time as a few days or as long as 3 months.

Neurogenic shock

Is caused by the absence of sympathetic activity from loss of supraspinal control and unopposed parasympathetic tone mediated by the intact vagus nerve.

Autonomic hyperreflexia

Is the syndrome of sudden massive reflex sympathetic discharge associated with a spinal cord injury at the thoracic level of T6 or above.

Herniated intervertebral disk

Compression of nerves causing radiating pain.

Ischemia with or without infarction

Brain abnormalities resulting from reduced blood flow.

Hemorrhage

Brain abnormalities resulting from bleeding.

Intercranial aneurysm

Is frequently asymptomatic. Cranial nerves III, IV, V, and VI are affected.

Arteriovenous malformation

Tangled vessels, rare congenital vascular lesion.

Migraine headache

Lasts 4–72 hours. Trigger factors; may or may not have an aura

Mechanism of migraine

Activation of trigeminal system, cortical spreading depression, brainstem nuclei activity.

Symptoms and diagnosis of migraines

When any two symptoms occur: unilateral head pain, pulsating pain, pain worsening with activity, moderate or severe pain. One of the following symptoms: nausea or vomiting, or both, photophobia, phonophobia

Cluster headache

Several attacks occurring during the day for days, followed by a long period of spontaneous remission. Trigger factors: Activation of the trigeminal system

Chronic paroxysmal hemicrania

Cluster-type headache with more frequent episodes but shorter duration. Primarily in women.

Tension-type headache

Mild-to-moderate bilateral headache with tight band or pressure sensation.

Infection and Inflammation of the Central Nervous System

Caused by bacteria, viruses, fungi, parasites, or mycobacteria.

Bacterial Meningitis

Throbbing headache increasing in severity, increasing photophobia, nuchal rigidity, positive Kernig sign, positive Brudzinski sign, projectile vomiting, neck stiffness.

Brain abscess treatment

Surgical aspiration or excision. Multiple or surgically inaccessible abscesses:antibiotics, often with steroidal therapy to treat cerebral edema. Intracranial pressure (ICP) may have to be managed.

Spinal cord abscess treatment

Surgical excision or aspiration. Antibiotics and support therapy.

Multiple Sclerosis

Progressive, chronic, inflammatory, demyelinating, autoimmune disorder of the Central Nervous System (CNS). Occurs in white and gray matter.

Plexus injuries

Nerve plexus involvement distal to the spinal roots but proximal to the formation of peripheral nerves.

Myasthenia gravis

Chronic autoimmune disease IgG. Defect in nerve impulse transmission at the neuromuscular junction AChR. Exertional fatigue and weakness that worsens with activity, improves with rest, and recurs with resumption of activity.

Meningiomas

Slow-growing, often encapsulated tumors arising from arachnoid (meningeal) cap cells in the dural coverings of the brain. Can cause seizures.

Brain metastases

symptoms include headache, seizures, and alterations in cognition, mental status, and behavior.

Spinal cord tumors

Gradual and progressive. Compressive syndrome (sensorimotor). Irritative syndrome (radicular). Syringomyelic syndrome (inflammation of the spinal cord).

Spinal cord tumor treatment

Surgery. Radiation. Chemotherapy. Hormonal therapy. Pain management.

Nervous system develops from a dorsal thickening of the ectoderm (neural plate) during approximately the middle of the

third gestational week.

Cranial deformities or craniostenosis

Premature closure of one or more of the cranial sutures during the first 18–20 months of life.

Microcephaly

Small brain is caused by reduced proliferation or accelerated apoptosis. Is not treatable. Can be true (primary) or secondary.

Cortical dysplasia

Is caused by defects in neuronal cell migration and subsequent abnormalities in connections between cells.

Epilepsy

is a recurrence of seizures and a disorder for which no cause can be found.

During a seizure oxygen and glucose are depleted at

60% higher than usual rate and lactate acid is accumulated

Generalized seizures

neurons bilaterally

Focal (partial) seizures

neurons unilaterally

Epilepsy syndromes

genetic/developmental cause

Unclassified epileptic seizures

etiology unknown

Status epilepticus

Is a medical emergency. Continuing/recurring seizures with incomplete recovery, unrelenting seizure activity that lasts 30 minutes or more and the main concern is hypoxia as oxygen decreases when having a seizure.

Clinical manifestations of Alzheimer’s dz

Progresses from mild short-term memory deficits and culminates in a total loss of cognition and executive functions; exhibits different stages. Includes forgetfulness; emotional upset; disorientation; confusion; lack of concentration; and declines in abstraction, problem solving, and judgment. Has an insidious onset.

Intercranial aneurysm treatment

Control hypertension. Surgery may be needed.

Clinical manifestations of cluster headache

Pain: unilateral, intense, tearing. Ptosis of ipsilateral eye. Nasal mucosa congestion. Referred pain in midface and teeth.