sleep Flashcards
Normal occurrence of REM
Adult
Child
Elderly
adult 4-5
child 4
elderly 3
sleep- wake cycle control in the brain
suprachiasmatic nucleus of hypothalamus
NREM sleep
(slow wave) non-rapid eye movements
REM sleep %
(fast wave) rapid eye movements [25%]
4 stages of NREM
Stage 1; Light Sleep [5%]
Stage 2; Deeper sleep [45%]
Stage 3-4 [25%]; Deepest , bed wetting, sleepwalking and night terror
Benzodiazepine decrease stage 4, useful for night terror and sleepwalking
Imipramine is used to treat enuresis since it decrease stage 4 sleep
REM Sleep characteristics
Every 90 min.
Beta wave ( like awake)
Increased and variable pulse
Dreams- you can tell the next moring
Tremendous loss of muscle tone- paralyzed
Erections
Decreases with benzodiazepines and old age
REM sleep is like sex: increase pulse , penile/clitoral erection, decrease with age
This condition is characterized by problem of insufficient sleep despite an adequate opportunity for sleep
insomnia
This is an intense and irresistible urge to sleep during daytime activities.
narcelopsy
This is an obstruction of respiratory air-ways during sleep
sleep apnea
In this condition REM sleep is entered directly from waking state and there is profound reduction of muscle tone and paralysis . This results fall on ground and inability to move
Cataplexy
Sleep Apnea due to extreme obesity
Pickwichian syndrome
This stage of sleep is related to bed-wetting
Stage 3 & Stage 4 of nonrem
Primary Motor Cortex“ motor strip”
Located in the precentral gyrus (area 4)
Composed of pyramidal cells whose axons make up the corticospinal tracts
Allows conscious control of precise, skilled, voluntary movements
Motor homunculus “little man” – represents areas of presentation of various organ in motor cortex
Primary motor cortex
damage
epileptic events
damage-stroke
epileptic events - jacksonian seizures
Premotor Cortex (area 6)
Located anterior to the precentral gyrus
Controls learned, repetitious, or patterned motor skills e.g. typing
Coordinates simultaneous or sequential actions
Involved in the planning and mental rehearsal of a movement
PYRAMIDAL (CORTICOSPINAL)
TRACT – Upper Motor Neurons
Most important output pathway from motor cortex to spinal cord
Fibers cross to opposite side –LCT
Fibers do not cross – VCT
Relay on interneurons and anterior horn cells of spinal cord
EXTRAPYRAMIDAL TRACTS
All tracts other than pyramidal tract Rubrospinal tract Pontine reticulospinal tarct Medullary reticulospinal tract Lateral vestibulospinal tract Tectospinal tract
Upper motor neuron lesions signs
Spastic paralysis, increased tendon reflexes, Bibinski sign +ve
Lower motor neuron lesion signs
Atrophy, flaccid paralysis, absent tendon reflex , Bibinski sign -ve
Coma
non-arousal due to damage to RAS
Decorticate Rigidity
Damage to brain above cerebellum and brainstem
Upper extremity flexion and lower extremity extension
Decerebrate Rigidity
Damage to brainstem and cerebral lesions
Arms and legs extension
Mechanical ventilation is required
Brown-Sequard’s Syndrome
Hemisection (transection on only one side) of spinal cord.
Gun shot wound
brown-sequard syndrome
Findings below the lesion:
Ipsilateral UMN signs (corticospinal tract)
Ipsilateral loss of fine touch, vibration, proprioception sense (dorsal column tract)
Contralateral loss of light touch, pain, temperature sense (spinothalamic tract)
Ipsilateral loss of all sensations at level of lesion.
LMN signs (e.g. flaccid paralysis) at level of lesion
horners syndrome
If lesion occurs above T1, presents with Horner’s syndrome
Horner’s Syndrome
Due to destruction of stellate (superior cervical) ganglion
Loss of sympathetic tone and predominant parasympathetic tone
Horner’s Syndrome
S/S (lesion above T1)
Ptosis (slight drooping of eyelids) Anhidrosis ( absence of sweating) Miosis (pupil constriction) Enophthalamos Flushing , temp Nasal congestion Ipsalateral of injury
Autonomic Dysreflexia / Autonomic Hyperreflexia Anesthesia considerations
Prevent further cord damage High dose steroid Head stabilization Monitor BP, CVP, PCWP Regional and deep general anesthesia
Autonomic Dysreflexia / Autonomic Hyperreflexia
Spinal cord injury at or above T6 (mid thoraric)
Unopposed sympathetic out flow norepinephrine, -hydroxylase and dopamine
Life threatening - hypertensive crisis, headache, vasoconstriction, skin pallor below the level of lesion
Bradycardia due to baroreceptor reflex, profuse sweating, vasodilation and skin flushing above the level of lesion
CEREBELLUM “Little Brain”
functions of cerebellum
Spinocerebellum
Spinocerebellum– control rate, force, range, and direction of movement
Layers of cerebellum
Granular layer
Purkinje cell layer – out puts are inhibitory
Molecular layer
Clinical disorders of cerebellum – ataxia
Lack of coordination , intention tremors
Poor execution of movement , inability to perform alternating movements
BASAL GANGLIA
Consists of striatum, globus pallidus, subthalamic nuclei and substantia nigra
Modulates thalamic out flow to motor cortex to plan and execute smooth movement
Many synaptic connections are inhibitory and use GABA
Lesion of subthalamic nucleus
Release of inhibition leads wild, flinging movements (hemiballismus)
Lesion of striatum
Release of inhibition leads to Huntington’s disease (dancing movements)
Lesion of substantia nigra
Destruction of dopamine producing neurons leads Parkinson’s disease
Over all inhibitory
Lead-pipe rigidity, tremors and reduced voluntary movements
Parkinson’s disease
decrease dopamine
Destruction of dopaminergic neurons of substantia nigra
Antipsychotic drugs- MCC
Resting Tremors, lead-pipe Rigidity, Akinesia ,Postural instability TRAP
Mask-like face, shuffling gait, pill rolling tremors
parkinsons treatment
Levodopa (dopamine cannot cross BBB) + carbidopa (DOPA decorboxylase inhibitor) combination - Sinemet ®
Dopamine-receptor agonists (bromocriptine, pramipexole)
MAO-B inhibitor ; Selegiline to increase dopamine activity
Amantadine (antiviral)
Anticholinergic
Benztropine
To counteract excessive action of acetylcholine
MAO-B Inhibitor
Selegiline (deprenyl) selectively inhibit MAO-B
increase dopamine level in brain
Use in Parkinson’s disease
Language
R Vs. L Hemisphere
Right hemisphere is dominant in facial expression
The left hemisphere is usually dominated with respect to language. Its lesion causes aphasia.
Brocas area
Damage to Broca’s Area causes motor aphasia, in which speech and writing is affected but understanding is intact.
Wernicke’s Area
Damage to Wernicke’s Area causes sensory aphasia, in which there is difficulty understanding written or spoken language- “word salad”
brocas vs. wernicke
Broca’s is nonfluent aphasia with intact comprehension (expressive aphasia). Wernicke’s is fluent aphasia with impaired comprehension (receptive aphasia)
short term memory
Short-term memory involves synaptic changes
long term memory
Long-term memory involves structural changes in nervous system and is more stable
Bilateral lesion of hippocampus block the ability to form new long-term memory
functions of cerebellum- vestibulocerebellum
Vestibulocerebellum– control balance and eye movements
CEREBELLUM “Little Brain”
functions of cerebellum
pontocerebellum
Pontocerebellum– planning and initiation of movement
autonomic hyperreflexia
NT outflow
Unopposed sympathetic out flow norepinephrine, B-hydroxylase and dopamine
