Neuro
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, followed by disorientation to place and impaired memory; recognition of self is lost last.
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 arousal (awakeness) with limited response to the environment; falls asleep unless verbally or tactilely stimulated; answers questions with minimum responses.
Stupor: Condition of deep sleep or unresponsiveness; person may be aroused or caused to open eyes only by vigorous and repeated stimulation; response is often withdrawal or grabbing at stimulus.
Coma: No verbal response to the external environment or to any stimuli; noxious stimuli such as deep pain or suctioning yields motor movement.
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 of near equal depth, resulting from trauma or compression to the medulla or from 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 (absence of motor and reflex responses). No spontaneous respirations (apnea). No brainstem function. Isoelectric (flat) 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 from direct ischemia and hypoxia. 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.
Tx of Acute confusional state: Identify the cause. May discontinue drugs. Pharmacologic/nonpharmacologic measures. Institute 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, postsurgical, 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: Dementia of the Alzheimer type (DAT), a senile disease complex. Specific diagnosis can only be made by postmortem examination. Clinical history, cognitive testing, course of the illness, laboratory tests, and brain imaging are used for diagnostic evaluation. Is the leading cause of dementia. Is irreversible. Greatest risk factors: age, family history. Familial: early or late onset
Pathophysiology of Alzheimer Dz: No known cause, Neurofibrillary tangles, Neuritic plaques, Degeneration of basal forebrain cholinergic neurons = Loss of acetylcholine
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.
Frontotemporal Dementia: Is a rare, severe degenerative disease of the frontal lobes. Produces death of tissue and dementia. Age of onset is younger than 60 years of age. Familial association.
Huntington disease (chorea): 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 (corpus striatum) 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 (PYRAMIDAL CELLS [MOTOR CORTEX]): 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 (VENTRAL HORN [SPINAL CORD], MOTOR NUCLEI [BRAINSTEM]): 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 clinical manifestations: Headache. Nervousness or anxiety. Irritability. Insomnia. Depression. Inability to concentrate, forgetfulness. Fatigability.
Postcuncussive syndrome Treatment: Reassurance and symptomatic relief. Close observation for
24 hours by a reliable individual to ensure that immediate intervention can be obtained if delayed effects become severe.
Primary spinal cord injury: Diaphragm function may be impaired because phrenic nerves exit at C3 to C5. Therefore an injury at C 4 might impair breathing.
Spinal shock: Is 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 (dysreflexia): 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: Pain radiating due to compression (called radiculopathy) along the nerve occurs.
Two types of brain abnormalities: Ischemia with or without infarction and Hemorrhage.
Intercranial aneurysm: Is frequently asymptomatic. Cranial nerves III, IV, V, and VI are affected.
Intercranial aneurysm treatment: Control hypertension. Surgery may be needed.
Rare congenital vascular lesions (cont.): Arteriovenous malformation tangled vessels.
Migraine headache: Lasts 4–72 hours. Trigger factors; may or may not have an aura
Mechanism of migraine: Activation of the trigeminal system, cortical spreading depression, and distinct activity of brainstem nuclei
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
Clinical manifestations of cluster headache: Pain: unilateral, intense, tearing. Ptosis of ipsilateral eye. Nasal mucosa congestion. Referred pain in midface and teeth.
Chronic paroxysmal hemicrania: Cluster-type headache occurring with more daily frequency (4–12 episodes per day) but with shorter duration (20–120 minutes). Primarily in women.
Tension-type headache: Most common. Mild-to-moderate bilateral headache with a sensation of a tight band or pressure around the head. Acute and chronic forms.
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. This is why with progressive seizure activity there is the potential for progressive brain injury and irreversible damage.
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.