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Sasha: Module 11 Neurology > CA Bates reading > Flashcards

Flashcards in CA Bates reading Deck (168)
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Motor: Chronic contralateral corticospinal-type weakness and spasticity. Flexion is stronger than extension in the arm, plantar flexion is stronger than dorsiflexion in the foot, and the leg is externally rotated at the hip.

Sensory: Contralateral sensory loss in the limbs and trunk on the same side as the motor deficits

DTR: increases

Ex of cause: cortical stroke

Cerebral Cortex (1)

Central Nervous System Disorders


MOtor Weakness and spasticity as above, plus cranial nerve deficits such as diplopia (from weakness of the extraocular muscles) and dysarthria

Sensory: Variable; no typical sensory findings

DTR: increased

ex of cause: Brainstem stroke, acoustic neuroma

Brainstem (2)

Central Nervous System Disorders


MOTor: Weakness and spasticity as above, but often affecting both sides (when cord damage is bilateral), causing paraplegia or quadriplegia depending on the level of injury

Sensory:Dermatomal sensory deficit on the trunk bilaterally at the level of the lesion, and sensory loss from tract damage below the level of the lesion

DTR: increased

ex of cause: Trauma, causing cord compression

Spinal Cord (3)

Central Nervous System Disorders


Motor: Slowness of movement (bradykinesia), rigidity, and tremor

Sensory: Sensation not affected

DTR: normal or decreased

ex of cause: Parkinsonism

Subcortical Gray Matter: Basal Ganglia (4)

Central Nervous System Disorders


Motor: Hypotonia, ataxia, and other abnormal movements, including nystagmus, dysdiadochokinesis, and dysmetria

Sensory: Sensation not affected

DTR: normal or decreased

ex of cause: Cerebellar stroke, brain tumor


Central Nervous System Disorders


Motor: Weakness and atrophy in a segmental or focal pattern; fasciculations

Sensory: Sensation intact

DTR: Decreased

ex of causes: Polio, amyotrophic lateral sclerosis

Anterior Horn Cell (1)

Peripheral Nervous System Disorders


Motor: Weakness and atrophy in a root-innervated pattern; sometimes with fasciculations

Sensory: Corresponding dermatomal sensory deficits

DTR: decreased

examples of cause: Herniated cervical or lumbar disc

Spinal Roots and Nerves (2)

Peripheral Nervous System Disorders


Motor: Weakness and atrophy in a peripheral nerve distribution; sometimes with fasciculations

Sensory: Sensory loss in the pattern of that nerve

DTR: decreased

ex of cause: trauma

Peripheral Nerve—Mononeuropathy (3)

Peripheral Nervous System Disorders


Motor: Weakness and atrophy more distal than proximal; sometimes with fasciculations

Sensory: Sensory deficits, commonly in stocking-glove distribution

DTR: decreased

Ex of cause:Peripheral polyneuropathy of alcoholism, diabetes

Peripheral Nerve—Polyneuropathy (4)

Peripheral Nervous System Disorders


Motor: Fatigability more than weakness

Sensory: Sensation intact

DTR: Normal

ex of cause: Myasthenia gravis

Neuromuscular Junction (5)

Peripheral Nervous System Disorders


Motor: Weakness usually more proximal than distal; fasciculations rare

Sensory: Sensation intact

DTR: Normal or decreased

ex of cause: Muscular dystrophy

Muscle (6)

Peripheral Nervous System Disorders


Although there are many causes of coma, most can be classified as either (2 types)

structural or metabolic


Arousal centers poisoned or critical substrates depleted

Toxic–Metabolic coma


Lesion destroys or compresses brainstem arousal areas, either directly or secondary to more distant expanding mass lesions.

Structural coma


Respiratory pattern:
If regular, may be normal or hyperventilation. If irregular, usually Cheyne-Stokes

Toxic–Metabolic coma


Pupillary size and reaction:
Equal, reactive to light. If pinpoint from opiates or cholinergics, you may need a magnifying glass to see the reaction.

May be unreactive if fixed and dilated from anticholinergics or hypothermia

Toxic–Metabolic coma


Level of consciousness:
Changes after pupils change

Toxic–Metabolic coma


causes: Uremia, hyperglycemia alcohol, drugs, liver failure hypothyroidism, hypoglycemia, anoxia, ischemia meningitis, encephalitis hyperthermia, hypothermia

Toxic–Metabolic coma


respiratory pattern: Irregular, especially Cheyne-Stokes or ataxic breathing. Also with selected stereotypical patterns like “apneustic” respiration (peak inspiratory arrest) or central hyperventilation

Structural coma


pupillary size and reaction: Unequal or unreactive to light (fixed)

Structural coma


Midposition, fixed—suggests

midbrain compression


Dilated, fixed—suggests

compression of CN III from herniation


LOC: changes BEFORE pupils change

Structural coma


Example of cause: Epidural, subdural, or intracerebral hemorrhage; cerebral infarct or embolus; tumor, abscess; brainstem infarct, tumor, or hemorrhage; cerebellar infarct, hemorrhage, tumor, or abscess

structural coma


Pupillary ____, ______, and ______ help to assess the cause of coma and to determine the region of the brain that is impaired.

Remember that unrelated pupillary abnormalities, including miotic drops for glaucoma or mydriatic drops for a better view of the ocular fundi, may have preceded the coma.

size, equality, and light reactions


suggest damage to the sympathetic pathways in the hypothalamus, or metabolic encephalopathy, a diffuse failure of cerebral function that has many causes, including drugs. Light reactions are usually normal.

Bilaterally small pupils (1–2.5 mm)


suggest a hemorrhage in the pons, or the effects of morphine, heroin, or other narcotics. The light reactions may be seen with a magnifying glass.

Pinpoint pupils (


Midposition fixed pupils

Pupils that are in the midposition or slightly dilated (4–6 mm) and are fixed to light suggest structural damage in the midbrain


may be due to severe anoxia and its sympathomimetic effects, as seen after cardiac arrest. They may also result from atropinelike agents, phenothiazines, or tricyclic antidepressants.

Bilaterally fixed and dilated pupils


may be due to cocaine, amphetamine, LSD, or other sympathetic nervous system agonists.

Bilaterally large reactive pupils