Neurology – Charts

Flashcard maker : Misty Porter
CNS : *Cerebral Cortex Lesion* : Motor Findings
– 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 thehip
CNS : *Cerebral Cortex Lesion* : Sensory Findings
Contralateral sensory loss in the limbs and trunk on the same side as the motor deficits
CNS : *Cerebral Cortex Lesion* : DTRs
increased DTRs
CNS : *Cerebral Cortex Lesion* : example of cause
cortical stroke
CNS : *Brainstem Lesion* : Motor Findings
weakness and spasticity plus cranial nerve deficits such as diplopia and dysarthria
CNS : *Brainstem Lesion* : Sensory Findings
variable; no typical sensory findings
CNS : *Brainstem Lesion* : DTRs
increased DTRs
CNS : *Brainstem Lesion* : Example of Cause
brainstem stroke, acoustic neuroma
CNS : *Spinal Cord Lesion* : Motor Findings
weakness and spasticity affecting both sides causing paraplegia or quadriplegia depending on the level of injury
CNS : *Spinal Cord Lesion* : Sensory Findings
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
CNS : *Spinal Cord Lesion* : Deep Tendon Reflexes
increased DTR
CNS : *Spinal Cord Lesion* : examples of causes
trauma, causing cord compression
CNS : *Subcortical Gray Matter* : Basal Ganglia Lesion : Motor Findings
slowness of movement (bradykinesia), rigidity, and tremor
CNS : *Subcortical Gray Matter* : Basal Ganglia Lesion : Sensory Findings
sensation not affected
CNS : *Subcortical Gray Matter* : Basal Ganglia Lesion : Deep Tendon Reflexes
DTR normal or low
CNS : *Cerebellar Lesion* : Motor Findings
hypotonia, ataxia, and other abnormal movements, including nystagmus, dysdiadochokinesis, and dysmetria
CNS : *Cerebellar Lesion* : Sensory Findings
sensation not affected
CNS : *Subcortical Gray Matter* : Basal Ganglia Lesion : Examples of Causes
parkinsonism
CNS : *Cerebellar Lesion* : Deep Tendon Reflexes
DTR normal or decreased
CNS : *Cerebellar Lesion* : examples of causes
cerebellar stroke, brain tumor
PNS : *Anterior Horn Cell Lesion* : Motor Findings
weakness and atrophy in a segmental or focal pattern; fasiculations
PNS : *Anterior Horn Cell Lesion* : Sensory Findings
sensation intact
PNS : *Anterior Horn Cell Lesion* : Deep Tendon Reflexes
DTR decreased
PNS : *Anterior Horn Cell Lesion* : Examples of Causes
polio, amyotrophic lateral sclerosis
PNS : *Spinal Roots and Nerves Lesions* : Motor Findings
weakness and atrophy in a root-innervated pattern; sometimes with fasiculations
PNS : *Spinal Roots and Nerves Lesions* : Sensory Findings
corresponding dermatomal sensory deficits
PNS : *Spinal Roots and Nerves Lesions* : Deep Tendon Reflexes
decreased DTRs
PNS : *Spinal Roots and Nerves Lesions* : Examples of Causes
herniated cervical or lumbar disc
PNS : *Peripheral Nerve – Mononeuropathy* : Motor Findings
weakness and atrophy in a peripheral nerve distribution; sometimes with fasiculations
PNS : *Peripheral Nerve – Mononeuropathy* : Sensory Findings
sensory loss in the pattern of that nerve
PNS : *Peripheral Nerve – Mononeuropathy* : Deep Tendon Reflexes
decreased DTR
PNS : *Peripheral Nerve – Mononeuropathy* : examples of causes
trauma
PNS : *Peripheral Nerve – Polyneuropathy* : Motor Findings
weakness and atrophy more distal than proximal; sometimes with fasiculations
PNS : *Peripheral Nerve – Polyneuropathy* : Sensory Findings
sensory deficits, commonly in stocking-glove distribution
PNS : *Peripheral Nerve – Polyneuropathy* : Deep Tendon Reflexes
decreased deep tendon reflexes
PNS : *Peripheral Nerve – Polyneuropathy* : Examples of Causes
peripheral polyneuropathy of alcoholism, diabetes
PNS : *Neuromuscular Junction Lesion* : Motor Findings
fatigability more than weakness
PNS : *Neuromuscular Junction Lesion* : Sensory Findings
sensation intact
PNS : *Neuromuscular Junction Lesion * : Deep Tendon Reflexes
normal DTRs
PNS : *Neuromuscular Junction Lesion* : Examples of Causes
Myasthenia Gravis
PNS : *Muscle Lesion* : Motor Findings
weakness usually more proximal than distal; fasiculations rare
PNS : *Muscle Lesion* : Deep Tendon Reflexes
normal or decreased DTRs
PNS : *Muscle Lesion* : Examples of Causes
muscular dystrophy
Anterior Cerebral Artery
Anterior Cerebral Artery
pink part
Anterior Choroidal Artery
Anterior Choroidal Artery
yellow part
Middle Cerebral Artery
Middle Cerebral Artery
green part
Posterior cerebral artery
Posterior cerebral artery
purple part
Prefrontal area
Prefrontal area
yellow part
Premotor area
light blue part
Primary Motor Cortex
light purple area
Motor speech (Broca's) area
Motor speech (Broca’s) area
dark purple area
Primary Somatic Sensory Cortex
Primary Somatic Sensory Cortex
Dark Green area
Somatic Sensory Association Area
Middle green area
Taste area
Taste area
yellowish green area
Primary Auditory Cortex
light pinkish area
Auditory Association Area
Auditory Association Area
Violet area
Sensory Speech (Wernicke’s area)
orange area
Reading comprehension area
teal area
Visual association area
Visual association area
middle pink area
Visual cortex
Visual cortex
red area
Vasodepressor or Vaovagal Syncope
– sudden peripheral vasodilation esp in skeletal muscles without compensatory risk in cardiac output; heart rate then blood pressure fall; often slow onset, slow offset
– brought on by a strong emotion such as fear or pain
– predisposing factors : fatigue, hunger, a hot humid environment are
– prodromal manifestations : restlessness, weakness, pallor, nausea, salivation, sweating, yawning
– prompt return of consciousness when lying down but pallor weakness nausea and slight confusion may persist for a time
Orthostatic (Postural) Hypotension
– Inadequate vasocontrictor reflexes in both arterioles and veins, with resultant venous pooling, decreasing cardiac outpat, and low blood pressure
– brought on by standing up
– parkinsons, shy-drager syndrome, lewy body disease diabetes, amyloidosis, antihypertensive vasodilator drugs; prolonged bed rest are predisposing factors
– associated with light headdedness and palpitations on standing up
– improvement with lying down
Cough Syncope
– neurally mediated, possible vagal stimulation
– brought on by severe paroxysm of coughing
– chronic bronchitis in a muscular man is a predisposing factor
– no prodromal manifestations except for cough
– prompt return to normal
Micturation Syncope
– vasovagal stimulation
– brought on by emptying the bladder after getting out of bed to void
– predisposing factors include nocturia
– prompt return to normal
Arrhythmias
– decreased cardiac output from cardiac ischemia, ventricular arrhythmias, prolonged QT syndrome, persistent bradycardia, infrafasicular block; often sudden onset; sudden offset
– precipitating factors include sudden change in rhythm
– predisposing factors include heart disease, aging decrease tolerance of abnormal rhythms
– prompt return to normal prolonged cerbral hypoperfusion cardiac arrest
Aortic Stenosis and Hypertrophic Cardiomyopathy
– vascular resistance falls with exercise, but cardiac output cannot rise due to outflow obstruction
– precipitating factors include exercise
– predisposing factors include cardiac disorders
– usually prompt return to normal
Myocardial Infarction
– sudden arrhythmia or decreased cardiac output
– predisposing factors include coronary artery disease
– prodromal manifestation is ischemic chest pain
Massive Pulmonary Embolism
– sudden hypoxia or decreased cardiac output
– variable precipitating factors including prolonged bed rest and clotting disorders
– DVT, bedrest, hypercoagulable states (SLE; cancer), protein S or C deficiency, antithrombin III deficiency, estrogen therapy
– dyspnea, pleuritic chest pain are prodromal manifestations
– recovery is related to time to diagnosis and treatment
Hypocapnia due to Hyperventilation
– constriction of cerebral blood vessels secondary to hypocapnia induced by hyperventilation
– precipitating factors : anxiety and panic disorders
– predisposing factors : anxiety
– dyspnea, palpitations, chest discomfort, numbness and tingling of the hands and around the mouth lasting for several minutes, consciousness is often maintained
– slow improvement as hyperventilation ceases
Hypoglycemia
– insufficient glucose to maintain cerebral metabolism; secretion of epinephrine contributes to symptoms; true syncope is uncommon
– variable precipitating factors including fasting
– insulin therapy and a variety of metabolic disorders are predisposing factors
– sweating, tremor, palpitations, hunger, headache, confusion, abnormal behavior, coma are prodromal
Hysterical Fainting from Conversion Reaction
– brought on through stressful situation
– hysterical personality traits are predisposing factors
Jacksonian Seizures
– tonic and then clonic movements that start unilaterally in the hand, foot, or face and spread to other body parts on the same side
– normal consciousness
Other motor focal seizures
– turning of the head and eyes to one side, or tonic and clonic movements of an arm or leg without the Jacksonian spread
– normal consciousness
Focal Seizures with autonomic symptoms
– a “funny feeling” in epigastrium, nausea, pallor, flushing, lightheadedness
– normal consciousness
Focal Seziures with subjective sensory or psychic phenomena
– numbness, tingling, simple visual, auditory, or olfactory hallucinations such as flashing lights, buzzing, or odors
– anxiety or fear; feelings of familiarity or unreality; dreamy states; fear or rage; flashback experiences; hallucinations
– normal consciousness
Focal Seizures with Impairment of Consciousness
– the seizure may or may not start with autonomic or psychic symptoms
– consciousness impaired and confusion
– automatisms included chewing, smacking the lips, walking about and unbuttoning clothes
– the patient may remember initial autonomic or psychic symptoms (aura) but is amnesic for the rest of the seizure
Focal Seizures that become generalized
– partial seizures that become generalized resemble tonic-clonic seizures; patient may not recall the focal onset
– recollection of an aura and unilateral neurologic deficit during the postictal period
Tonic Clonic (grand mal) Seizures : Clinical Manifestations
– sudden loss of consciousness sometimes with a cry
– body stiffens into tonic extensor rigidity
– breathing stops and the person becomes cyanotic
– clonic phase of rhythmic muscular contraction follows
– breathing resumes and is often noisy with excessive dalivation
Generalized Seizures : Postictal State
confusion, drowsiness, fatigue, headache, muscular aching, and sometimes the temporary persistence of bilateral neurologic deficits such as hyperactive reflexes
amnesia of the seizure and no recollection of aura
Absence Seizures : Clinical Manifestations
sudden brief lapse of consciousness with momentary blinking, staring, or movements of lips and hands but no failing
– typical lasts less than 10 seconds and stop abruptly
– atypical may last more than 10 seconds
Absence Seizures : Postictal State
no aura recalled
Myoclonic Seizures : Clinical Manifestations
sudden, brief rapid jerks, involving the trunk or limbs
Myoclonic Attack : Clinical Manifestations
sudden loss of consciousness with falling but no movements; injury may occur
Myoclonic Attack : Postictal State
either a prompt return to normal or brief period of confusion
Resting (Static) Tremors
Resting (Static) Tremors
prominent at rest and may decrease or disappear with voluntary movement; common, relatively slow, fine, pill-rolling tremor of parkinsonism, about 5 per second
Postural Tremors
appear when affected part is actively maintaining a posture; examples include the fine rapid tremor of hyperthyroidism, anxiety, fatigue
Intention Tremors
Intention Tremors
absent at rest, appear with movement and often get worse as the target gets closer; include disorders of cerebellar pathways, as in MS, or any other disease of the cerebellum
Oral-Facial Dyskinesias
Oral-Facial Dyskinesias
rhythmic, repetitive, bizarre movements that chiefly involve the face, mouth, jaw, and tongue; grimacing, pursing of the lips, protrusions of the tongue, opening and closing of the mouth, and deviations of the jaw
Tics
Tics
brief, repetitive, stereotyped coordinated movements occurring at irregular intervals i.e., tourette’s
Dystonia
grotesque twisted postures may result
Athetosis
Athetosis
slower more twisting and writhing movements that have a large amplitude; commonly involve the face and distal extremities
Chorea
Chorea
brief, rapid, jerky, irregular, and unpredictable; occur at rest or interrupt normal coordinated movements; they seldom repeat themselves; face, head, lower arms, and hands are often involved
Wernicke’s Aphasia
– fluent often rapid and effortless speech
– inflection and articulation are good but sentences lack meaning and words are gibberish
– may be totally incomprehensible
– word comprehension, repetition, naming, reading comprehension, writing all impaired
– lesion located in posterior superior temporal lobe
Broca’s Aphasia
– nonfluent
– slow with few words and laborious effort
– inflection and articulation are impaired but words are meaningful
– small grammatical words often dropped
– fair word and reading comprehension
– impaired repetition, writing, and naming
– lesion located in posterior inferior frontal lobe
Nystagmus
rhythmic oscillation of eyes; caused by vision impairment early in life, disorders of the labyrinth and cerebellar system, and drug toxicity; can occur normally when watching rapidly moving objects
Nystagmus – Lateral Gaze
nystagmus may be present in all directions but only accentuates in deviation of eyes as seen in extreme lateral gaze left or right; normal people show signs of slight nystagmus in lateral gaze
Left-beating nystagmus
if eyes jerk quickly to patients left and slowly to the right
Pendular nystagmus
nystagmus consisting only of coarse oscillations without quick and slow components
Horizontal nystagmus
Vertical nystagmus
Rotary Nystagmus
CN VII Peripheral Lesion
CN VII Peripheral Lesion
paralyzes the entire right side of the face including forehead; right eye does not close and the eyeball rolls up; forehead not wrinkled and eyebrow not raised
CN VII Central Lesion
CN VII Central Lesion
Eye closes with slight weakness and forehead is wrinkled with eyebrow raised
Lesions Producing Spastic Muscle Tone
Upper motor neuron or corticospinal tract systems
Spasticity
– increased muscle tone that is greater when passive movement is rapid and less when passive movement is slow; greater at the extremes or movement arc; sudden limb reflexes
– seen in stroke
Lesions Producing Rigid Muscle Tone
Basal Ganglion System
Lead Pipe Rigidity
increased resistance that persists throughout the movement arc independent of rate of movement
Cogwheel Rigidity
rigidity with flexion and extension of the wrist and forearm, a superimpose rachetlike jerkiness
seen in parkinson’s patients
Lesions Producing Flaccid Muscle Tone
lower motor neuron system (from anterior horn cell to peripheral nerves)
Flaccidity
loss of muscle tone causing loose and floppy limbs; limbs may be hyperextensible or even flail like
seen in Guillain Barre syndrome
Lesions producing paratonia muscle tone
both hemispheres, usually in the frontal lobes
Paratonia
sudden change in tone with passive ROM
Paratonia – Mitghen
sudden loss of tone that increases the ease of motion
Paratonia – Gegenhalten
sudden increase in tone making motion more difficult
Spastic Hemiparesis
Spastic Hemiparesis
– corticospinal tract lesion in stroke
– poor control of flexor muscles during swing phase
– arm is flexed, immoble, and held close to side with elbow, wrists, and interphalangeal joints flexed
– leg extensors spastic
– ankle plantar flexed and inverted
– pts may drag toe, circle leg stiffly outward and forward or lean trunk to contralateral side to clear affected leg during walking
Scissors Gait
Scissors Gait
– spinal cord disease
– caused by bilateral lower extremity spasticity including adductor spasm and abnormal proprioception
– stiff gait with slow leg advancement
– thighs tend to cross forward on each other with each step
– steps are short
– pts appear to be walking through water
– common in cerebral palsy
Steppage Gait
– foot drop
– secondary to peripheral motor unit disease
– pts drag the feet or light them high with knees flexed and slap them down onto the floor
– walking up stairs
– cannot walk on heels
– tibalis anterior and toe extensors are weak
Parkinsonian Gait
– basal ganglia defects
– posture is stooped with flexion of head, arms, hips, and knees
– pts are slow getting started
– short shuffling steps with involuntary hastening
– limited arm swings
Cerebellar Ataxia
Cerebellar Ataxia
– dx of cerebellum or associated tracts
– gait is staggering, unsteady, and wide based with exaggerated difficulty on turns
– pts cannot stand steadily w feet together whether eyes are opened or closed
– nystagmus, dysmetria, and intention tremor
Sensory Ataxia
Sensory Ataxia
– loss of position sense in legs
– gait is unsteady and wide based
– pts throw their feet forward and outward and bring them down first on heels then on toes with double tapping sound
– watch grown
– with eyes closed they cannot stand steadily with feet together (positive Romberg)
Toxic Metabolic Comas
arousal centers poisoned or critical substrates depleted
Toxic Metabolic Comas : Respiratory Pattern
if regular may be normal or hypervenilation; if irregular usually Cheyne-Stokes
Toxic Metabolic Comas : Pupillary size and reaction
– equal and reactive to light
– pinpoint = opiates/cholinergics; need magnifying glass to see reaction
– fixed and dilated = anticholinergics/hypothermia
Toxic Metabolic Comas : Causes
– uremia
– hyperglycemia
– alcohol
– drugs
– liver failure
– hypothyroidism
– hypoglycemia
– anoxia
– ischemia
– meningitis
– encephalitis
– hyperthermia
– hypothermia
Structural Coma
lesion destroys or compresses brainstem arousal areas either directly or secondary to more distant expanding mass lesions
Structural Coma : Respiratory Pattern
– irregular especially Cheyne-Strokes or ataxic breathing
Structural Coma : Pupillary Size and Reaction
– unequal or unreactive to light
– midposition, fixed = midbrain compression
– dilated, fixed = compression of CN III from herniation
Structural Coma : Causes
– epidural, subdural, or intracerebral hemorrhage
– cerebral infarct or embolus
– tumor or abscess
– brainstem infarct, tumor, or hemorrhage
– cerebellar infarct, hemorrhage, tumor, or abscess
Glasgow Coma Scale
higher number = more aware
Bilaterally Small Pupils
Bilaterally Small Pupils
– 1-2.5 mm
– suggest damage to the sympathetic pathways in the hypothalamus or metabolic encephalopathy
– diffuse failure of cerebral function that has many causes including drugs
– light reactions are usually normal
Pinpoint Pupils
– <1mm
– suggests a hemorrhage in the pons or the effects of morphine, heroin, or other narcotics
– light reaction may be seen w magnifying glass
Midposition Fixed Pupils
Midposition Fixed Pupils
– slightly dilated and fixed to light
– suggest structural damage in the midbrain
Bilaterally fixed and dilated pupils
– may be due to severe anoxia and its sympathomimetic effects as seen after cardiac arrest
– may also be seen from atropinelike agents, phenothiazines, or tricyclic antidepressants
Bilaterally large reactive pupils
may be due to cocaine, amphetamine, LSD or other sympathetic nervous system agonists
One Large Pupil
herniation of the temporal lobe causing compression of the oculomotor nerve and midbrain; most commonly seen in diabetic pts with infarction of CN III
Decorticate Rigidity (Abnormal Flexor Response)
– upper arms are flexed tight to the sides with elbows, wrists, and fingers flexed
– legs are extended and internally rotated
– feet are plantar flexed
– implies a destructive lesion of the corticospinal tracts within or very near the cerebral hemispheres
– when unilateral = chronic spastic hemiplegia
Hemiplegia (Early)
– sudden unilateral brain damage involving the corticospinal tract
– one-sided paralysis
– flaccid in early course with spasticity developing larger
– paralyzed arm and leg are slack falling loosely without tone
– spontaneous movements or responses are limited to opposite side
– leg may lie externally rotated
– one side of lower face is paralyzed and that cheek puffs on expiration
– both eyes may be turned away from paralyzed side
Decerebrate Rigidity (Abnormal Extensor Response)
– jaws are clenched and neck is extended
– arms are adducted and stiffly extended at the elbows with forearms pronated, wrists and fingers flexed
– legs are stiffly extended at the knees with feet plantar flexed
– may occur spontaneously or only in response to external stimuli (light, noise, or pain)
– caused by a lesion in diencephalon, midbrain, or pons OR by metabolic disorders such as hypoxia and hypoglycemia

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