Neuro Flashcards
Neural Development
Notochord induce ectoderm to differentiated –> neuroectoderm –> neural plate –> neural tube and NCC
Notochord becomes nucleus pulpsus
Alar plate (dorsal)- sensory, regulated by TGFB (BMP)
Basal plate (ventral: motor, regulated by SHH
Prosencephalon
Telencephalon –> cerebral hemispheres and basal ganglia (walls) and lateral ventricles (cavities)
Diencephalon –> Thalamus, hypothalamus, retina (walls) and third ventricle (cavity)
Mesencephalon
Midbrain (walls) Cerebral aqueduct (cavities)
Rhomboencephalon
Metencephalon –> pons and cerebellum (walls) and upper part of fourth ventricle (cavity)
Myelencephalon –> medulla (walls) and lower part of fourth ventricle (cavity)
CNS origin
Neuroepithelia in neural tube –> CNS, ependymal cells, oligodendrocytes, astrocytes
PNS origin
NCC –> PNS, Schwann cells, glia, melanocytes, adrenal medulla
Microglia origin
Mesoderm
Neural tube defects
Neuropores fail to fuse (4th week) –> persistent connection between amniotic cavity and spinal canal
Associated with maternal DM and low folate
High AFP and acetylcholinesterase
Spinal bifida occulta
Failure of causal neuropore to close, but no herniation
seen at lower vertebral levels
Dura intact
Associated tuft of hair or skin dimple at level of bony defect
Meningocele
Meninges herniate through bony defect
Myelomeningocele
Meninges and neural tissue herniate through bony defect
Myeloschisis
Exposed, unfused neural tissue without skin covering
Anencephaly
failure of rostral neuropore to close –> no forebrain, open calvarium
polyhydramnios
Holoprosencephaly
Failure of embryonic forebrain to separate into 2 cerebral hemispheres (weeks 5-6)
Mutations in SHH
Associated with other midline defects (cleft lip, cyclopia)
increased risk of pituitary dysfunction
Associated with Patau
Lissencephaly
failure of neuronal migration resulting in smooth brain that lacks sulci and gyri
associated with microcephaly, ventriculomegaly
Chiari I malformation
Ectopia of cerebellar tonsils inferior to foramen magnum
Congenital, asymptomatic in children
Adult- HA, cerebella symptoms
Associated with syringomyelia
Chiari II malformations
Herniation of cerebellar vermis and tonsils through foramen magnum with aqueductal stenosis –> noncommunicating hydrocephalus
Associated with lumbosacral myelomeningocele
MORE SEVERE
presents earlier in life
Dandy Walker malformation
agenesis of cerebellar vermis –> cystic enlargement of 4th ventricle that fills the enlarged posterior fossa
Associated with noncommunicating hydrocephalus, spina bifida.
Syringomyelia
Cystic cavity within central canal of spinal cord
Fibers crossing in anterior white commissure damaged first
cape like bilateral symmetrical loss of pain and temperature sensation of UE
Associated with Chiari I and scoliosis
Tongue Development
1st and 2nd pharyngeal arches for anterior 2/3 (CNV3 and CN VII)
3rd and 4th pharyngeal arches form posterior 1/3 (CNIX and CNX)
motor innervation via CNXII to hyoglossus, genioglossus and styloglossus
Motor innervation via CNX to palatoglossus
Neurons
Signal tranmission
Permanent- do not divide in adults
Neuron markers: neurofilament proteins, synaptophysin
Astrocytes
common glial cell type in CNS Physical support, repair, extracelluar K buffer, remove excess NT BBB Derived from neuroectoderm Marker: GFAP
Microglia
Phagocyte cells of CNS
mesoderm
Not stained via Nissl
HIV infected –> dementia
Ependymal cells
ciliated columnar glial cells line ventricles and central canal of spinal cord
Apical surfaces are covered in cilia and microvilli
Choroid plexus –> produce CSF
Myelin
increase conduction velocity of signals –> saltatory conduction of AP at nodes of Ranvier
Synthesized by oligodendrendrocytes or schwann cells
Schwann cells
promote axonal regeneration
NCC
injured in Guillain barre
Oligodendrocytes
Myelinate axons of neurons in CNS Predominate glial cell in white matter Neuroectoderm fried egg appearance injured in MS, PML and leukodystrophies
Free Nerve endings
all skin, epidermis, viscera
sense pain and temp
Adelta- fast myelinated fibers
C- slow unmyelinated
Meissner Corpuscles
large myelinated fibers adapt quickly
glabrous skin (no hair)
dynamic, fine/light touch position sense, low frequency vibrations
Pacinian corpuscles
large myelinated fibers adapt quickly
deep skin layers, ligaments, joints
high frequency vibration, pressure
Merkel discs
large myelinated fibers adapt slowly
finger tips, superficial skin
pressure deep static touch, position sense
Ruffini corpuscles
Dendritic endings with capsule, adapt slowly
finger tips, joints
pressure, slippage of objects along surface of skin, joint angle change
Peripheral Nerve structure
Endoneurium- thin supportive connective tisse that ensheathes and supports individual myelinated nerve fibers
Perineurium- surround fascicle of nerve fibers
epineurium- dense connective tissue that surrounds entire nerve
Chromatolysis
reaction of neuronal cell body to axonal injury
high protein synthesis –> round cellular swelling, displacement of nucleus to periphery, dispersion of Nissl substance throughout cytoplasm
Proximal to injury –> axon retracts and cell body sprouts new protrusions that grow for reinnervation
Wallerian degeneration
disintegration of the axon and myelin sheath distal to the site of axonal injury with macrophages removing debris
ACh synthesis
Basal nucleus of Meynert
Dopamine synthesis
Ventral tegmentum, SNc
GABA synthesis
Nucleus acumbens
NER synthesis
locus ceruleus
5HT synthesis
Raphe nuclei
Dura mater
thick outer layer closes to skull
Mesoderm
potential space between dura mater and skull contain fat and blood vessels (epidural space)
Arachnoid mater
middle layer, contains web like connections
NCC
CSF flow below arachnoid mater
Pia mater
thin fibrous inner layer that adheres to brain and spinal cord
NCC
BBB
prevent circulating blood substances from reaching the CSF.CNS
Tight junctions
Basement Membrane
Astrocyte foot processes
Glucose and AA cross slowly by carrier mediated transport
lipid soluble substances cross rapidly
Vomiting center
coordinated by NTS in medulla receives info from CTZ , GI tract, vestibular system and CNS
CTZ receive input from muscarinic, DA, histamine, 5HT and NK1 receptors
Sleep physiology
suprachiasmatic nucleus regulated by light
control nocturnal release of ACTH, prolactin, melatonin, NE
Alcohol, benzos, and barbs associated with low REM and N3 sleep
Awake eyes open
alert active mental concentration
Beta waves
Awake eyes closed
alpha waves
N1
light sleep
theta waves
N3
deepest non REM sleep
sleepwalking, night terrors, bedwetting
delta waves
N2
deeper sleep
bruxism
sleep spindles and K complex
REM
loss of motor tone, increase brain O2, ACh dreaming, nightmares, penile tumescence memory processing PPRF --> extraocular movements every 90 minutes beta waves old ppl- decreased REM time and N3 Depression- increased REM time, low REM latency, low N3 Narcolepsy- low REM latency
Hypothalamus
Maintain homeostasis by regulating Thirst and water balance, controlling adrenohypophysis and neurohypophysis release of hormones produced in the hypothalamus and regulating hunger, ANS, temperature and sexual urges
Lateral nucleus
Hypothalamus
hunger destruction –> anorexia, failure to thrive
Stimulated by ghrelin, inhibited by leptin
Ventromedial nuclues
Hypothalamus
Satiety
Destruction –> hyperphagia
Stimulated by leptin
Anterior nucleus
Hypothalamus
cooling PNS
Posterior Nucleus
Hypothalamus
heating
SNS
Suprachiasmatic nucleus
Hypothalamus
circadian rhythm
Supraoptic and paraventricular nuclei
Hypothalamus
synthesize ADH and oxytocin
Preoptic nuclei
Hypothalamus
Thermoregulation, sexual behavior, Releases GnRH
Failure of GnRH neurons to migrate to olfactory bulb –> Kallmann syndrome
Thalamus
Major relay for all ascending sensory information except olfaction
Ventral Posterolateral nucleus
Thalamus
input- spinothalamic and dorsal columns medial lemniscus
Vibration, pain, pressure, proprioception, light touch, temp
Destination- Primary somatosensory cortex
Ventral posteromedial nucleus
Thalamus
Input- trigeminal and gustatory
Face sensation, taste
Destination- primary somatosensory cortex
Lateral geniculate nucleus
Thalamus
Input- CNII, optic chiasm, optic tract
Vision
Destination- primary visual cortex
Medial geniculate nucleus
Thalamus
Input- superior olive and inferior colliculus of tectum
Hearing
Destination- auditory cortex of temporal lobe
Ventral lateral nucleus
Thalamus
Input- Cerebellum, basal gnaglia
Motor
Destination- motor cortex
Limbic system
Emotion, long term memory, olfaction, behavior modulation, ANS function
hippocampus, amygdala, mammillary bodies, anterior thalamic nuclei, cingulate gyrus, entorhinal cortex
Feeding, fleeing, fighting, feeling, sex
Mesocortical DA pathway
decreased activity –> negative symptoms
Mesolimbic DA pathway
increased activity –> positive symptoms
Nigrostriatal DA pathway
decreased activity –> extrapyramidal symptoms (dystonia, akathisia, parkinsonism, tardive dyskinesia)
Tuberoinfundibular DA pathway
decreased activity –> increase prolactin –> decrease libido, sexual dysfunction, galactorrhea, gynecomastia
Cerebellum
modulate movement, aids in coordination and balance
Lateral lesions –> affect voluntary movement of extremities. Fall toward injured side
Medial lesions –>truncal ataxia, nystagmus, head tilting. Bilateral motor deficits affecting axial and proximal limb musculature
Basal ganglia
voluntary movement and adjusting posture
Striatum = putamen (motor) + Caudate (cognitive)
Lentiform= putamen + globus pallidus
Direct Basal ganglia pathway
SNc input to the striatum via nigrostriatal DA pathway –> release GABA –> inhibit release from GPi –> disinhibit thalamus –> increase motion
Indirect Basal ganglia pathway
SNc input to the striatum via nigrostriatal DA pathway –> release GABA –> disinhibit STN via GPe inhibition and stimulate GPi –> inhibit thalamus –> decrease motion
Cerebral perfusion
Relies o tight autoregulation driven by PCO2
Also relies on MAP, ICP (low BP/ high ICP –> decreased cerebral perfusion pressure
Therapeutic Hyperventilation
decrease PCO2 –> vasoconstriction –> decrease cerebral blood flow –> decrease ICP
Used to treat acute cerebral edema unresponsive to other interventions
Homunculus
Topographic representation of motor and sensory areas in cerebral cortex
Distorted appearance is due to certain body regions being more richly innervated and thus have high cortical representation
Dural venous sinuses
Large venous channels that run through the periosteal and meingeal layers of the dura mater. Drain blood from cerebral veins and receive CSF from arachnoid granulations
Empty into internal jugular V
Venous sinus thrombosis
high ICP
may lead to venous hemorrhage
Associated with hypercoaguable states
Ventricular system of the brain
Lateral –> 3rd via right and left interventricular foramina of monroe
3rd –> 4th via cerebral aqueduct of Sylvius
4th –> subarachnoid space via foramina of Luschka (lateral) and Magendie (medial)
CSF production
via choroid plexus in lateral and 4th ventricles
Travel to subarachnoid space
reabsorbed by arachnoid granulations
drain into dural venous sinuses
Cranial Nerves in brain
4 CN above pons
4 CN via pons
4 CN in medulla
4 CN medial (3, 4, 6, 12)
Pineal gland
melatonin secretion, circadian rhythm
Superior colliculi
direct eye movements to stimuli or objects of interest
Inferior colliculi
auditory
Olfactory N
CN1
Smell
Sensory
Optic N
CN2
sight
Senory
Oculomotor
CN 3
Eye movement- SR, IR, MR, IO
pupillary constriction, accomodation, eyelid opening
Motor
Trochlear N
CN 4
eye movement SO
Motor
Trigeminal
CN 5
Mastication, facial sensation, somatosensation from anterior 2/3 tongue, dampen loud noises (tensor tympani)
sensory and motor
Abducens
CN6
Eye movement LR
Motor
Facial N
CN 7
facial movement, taste from anterior 2/3 tongue, lacrimation, salivation, eye closing, auditory volume modulation
sensory and motor
Vestibulocochlear N
CN 8
hearing, balance
sensory
Glossopharyngeal N
CN 9
Taste and sensation from posterior 1/3 tongue, swallowing, salivation, monitor carotid body and sinus chemo and baroreceptors and elevation of pharynx
sensory and motor
Vagus N
CN 10
taste from supraglottic region, swalloing, soft palate elevation, midline uvula, talking, cough reflex, PNS to thoracoabdominal viscera, monitor aortic arch chemo and baroreceptors
sensory and motor
Accessory N
CN 11
Head turning, shoulder shrug
Motor
Hypoglossal N
CN 12
tongue movement
motor
Nucleus Tractus Solitarius
Vagal nuclei
visceral sensory information
CN 7, 9, 10
Nucleus ambiguous
Vagal nuclei
motor innervation of pharynx, larynx, upper esophagus
CN 9, 10, 11
Dorsal motor nucleus
Vagal nucleus
sends PNS to heart, lungs, upper GI
CN 10
Corneal reflex
V1 ophthalmic (nasociliary) to bilateral CN 7
Lacrimation reflex
V1 –> 7
Jaw jerk
V3 (sensory from masseter) –> V3 (motor- masseter)
Pupillary reflex
CN 2 –> CN 3
Gag reflex
CN 9 –> CN 10
Cough reflex
CN 10 –> CN 10
Mastication Muscles
Close jaw- Masseter, temporalis, medial pterygoid
Open jaw - lateral pterygoid
Innervated by V3
Spinal cord ends in adults at
lower border of L1-L2 vertebrae
Subarachnoid space extends to
lower border of S2
Lumbar puncture
between L3-L4 or L4-L5 Skin Fascia, fat supraspinous L interspinous L Ligamentum Flavum Epidural space dura mater arachnoid mater subarachnoid space
Dorsal Column
Ascending
Pressure, vibration, fine touch, propiception
Sensory N ending –> bypass pseudounipolar cell body in DRG –> enter spinal cord –> ascend IPSILATERAL in dorsal column –> NUCLEUS GRACILIS, NUCLEUS CUNEATUS –> decussates in medulla –> ascends CONTRALATERALLY as medial lemniscus –> VPL
Spinothalamic tract
Ascending
Lateral - pain, temperature
Anterior- crude touch, pressure
Sensory N ending –> bypass pseudounipolar cells body in DRG –> enter spinal cord –> IPSILATERAL gray matter –> decussates in spinal cord as the anterior white comissure –> ASCEND CONTRALTERALLY –> VPL
Lateral Corticospinal tract
Descending
Voluntary movement of contralateral limb
UMN: cell body in primary motor cortex –> descend IPSILATERALLY, most fibers decusssate at caudal medulla –> DESCEND CONTRALATERALLY –> cell body of anterior horn –> LMN (leave spinal cord)
Achilles reflex
S1
Patellar reflex
L4
Biceps and brachioradialis reflex
C5
Triceps reflex
C7
Cremasteric reflex
L1, L2
Anal wink reflex
S3, S4
Primitive reflexes
CNS reflexes present in a healthy infant but absent in adults
disappear within first year
Inhibited by mature frontal lobe
Moro reflex
Primitive reflex
hang on for life
abduct/extend arm when startled then draw together
Rooting reflex
Primitive reflex
movement of head toward one side if cheek or mouth in stroked
Sucking reflex
Primitive reflex
sucking response when rook of mouth is touched
palmar reflex
Primitive reflex
curling fingers if palm is stroked
Plantar reflex
Primitive reflex
dorsiflexion of large toe and fanning of other toes with plantar stimulation
Babinski sign in adults = lesion in UMN
Galant reflex
Primitive reflex
stroking along one side of spine while newborn is in ventral suspension causes lateral flexion of lower ody toward stimulated side
C2 Dermatome
Posterior half of skull
C3 Dermatome
High turtleneck shirt
Diaphragm, gallbladder pain referred to right shoulder via phrenic
C4 Dermatome
low collar shirt
C6 Dermatome
thumbs
T4 Dermatome
Nipple
T7 Dermatome
xiphoid process
T10 Dermatome
umbilicus
L1 Dermatome
Inguinal L
L4 Dermatome
kneecaps
S2, S3, S4 Dermatomes
sensation of penile and anal zones
Frontal lobe lesion
Disinhibition and deficits in concentration, orientation, judgement
may have reemergence of primitive reflexes
Frontal eye fields lesions
Destructive lesions (MCA stroke) eyes look toward brain lesion
Paramedian pontine reticular formation lesion
Eyes look away from brain lesion
Medial longitudinal fasciculus lesion
internuclear ophthalmoplegia (impaired adduction of ipsilateral eye, nystagmus of contralateral eye with abduction) Multiple sclerosis
Dominant parietal cortex lesion
Agraphia, acalculia, finger agnosia, left- right disorientation
Gerstmann syndrome
Nondominant parietal cortex Lesion
Agnosia of the contralateral side of he world
Hemispatial neglect syndrome
Hippocampus lesion
anterograde amnesia, inability to make new memories
Basal ganglia lesion
May result in tremor at rest, chorea, athetosis
Parkinsons, huntington, wilson
Subthalamic nucleus lesion
Contralateral hemiballismus
Mammillary bodies lesion
Wernicke Korsakoff syndrome- confusion, ataxia, nystagmus, ophthalmoplegia, memory loss, confabulation, personality changes
Alcoholics
Amygdala lesion
Kluver Bucy Syndrome- disinhibited behavior
HSV 1 encephalitis
Doral Midbrain lesion
Parinaud syndrome- vertical gaze palsy, pupillary light near dissociation, lid retraction, convergence retraction nystagmus
stroke, hydrocephalus, pinealoma
Reticular activating system lesion
reduced levels of arousal and wakefulness
Coma
Cerebellar hemisphere lesion
intention tremor, limb ataxia, loss of balance, damage to the cerebellum –> ipsilateral deficits
Cerebellar vermis lesions
truncal ataxia, nystagmus
chronic alcohol use
Red nucleus lesion
decorticate posturing- lesion above red nucleus –> flexion of upper extremities and extension of lower extremities
Decerebate posturing- lesion at or below red nucleus –> extension of upper and lower extremities (WORSE PROGNOSIS)
Ischemic brain disease/ stroke
irreversible injury begins after 5 minutes of hypoxia
most vulnerable = hippocampus, neocortex, cerebellum, watershed areas
12- 24 hours post stroke
eosinophilic cytoplasm and pyknotic nuclei
24-72 hours post stroke
necrosis and neutrophils
3-5 days post stroke
macrophages
1-2 weeks post stroke
reactive gliosis and vascular proliferation
> 2 weeks post stroke
glial scar
Ischemic stroke
block vessels –> infarction –> liquefactive necrosis
Thrombotic- clot formation at site of infarction (MCA), atherosclerotic plaque
Embolic- embolus from another part of body. A- fib, carotid artery stenosis, DVT, infective endocarditis
Hypoxic- hypoperfusion. Cardiovascular surgery. watershed areas
T(x): tPA within 3-4.5 hours, aspirin
Transient ischemic attack
brief, reversible episode of focal neruo dysfunction without acute infarction with resolution in <15 minutes
Neonatal intraventricular hemorrhage
bleeding into ventricles
increased risk in premature, low birth weight infants
originate in germinal matrix.
Due to reduced glial fiber support and impaired autoregulation of BP in premature infants
altered level of consciousness, bulging fontanelle, hypotension, seizures, coma
Epidural hematoma
rupture of middle meningeal A
secondary to skull fracture (pterion)
transient loss of consciousness –> recovery –> rapid deterioration
Scalp hematoma and intracranial expansion –> transtentorial herniation –> CN III palsy
Subdural hematoma
Rupture of bridging veins
shaken babies
crescent shaped hemorrhage that crosses the suture lines
Subarachnoid hemorrhage
bleeding due to trauma or rupture of an aneurysm or arteriovenous malformation
WORST HA OF LIFE
bloody or yellow lumbar puncture
Vasospasm or rebleed can occur, use nimodipine
Intraparenchymal hemorrhage
caused by systemic HTN, amyloid angiopathy, vasculitis, neoplasm
secondary to reperfusion injury
Putamen of basal ganglia, thalamus, pons and cerebellum
Middle cerebral A
motor and sensory cortices- upper limb and face –> CONTRA paralysis and sensory loss in face and upper limb
Temporal lobe and frontal lobe- aphasia and right superior quadrant visual defect if in dominant hemisphere. Hemineglect if affects nondominant
Anterior cerebral A
motor and sensory cortices- lower limb–> CONTRA paralysis and sensory loss- lower limb, urinary incontinence
Lenticulostriate A
Striatum, internal capsule –> CONTRA paralysis. Absence of cortical signs
Lacunar infarcts
Anterior spinal A
Corticospinal tract –> CONTRA paralysis- upper and lower limbs
Medial lemniscus –> decreased CONTRA propioception
Caudal Medulla- hypoglossal N –> IPSI hypoglossal dysfunction
Medial Medullary syndrome
caused by infarct of paramedian branches of ASA or vertebral A
Posterior Intferior Cerebellar A
Lateral medulla
Nucleus ambiguous –> dysphagia, hoarseness, no gag reflex, hiccups
Vestibular nuclei –> vomiting, vertigo, nystagmus
Lateral spinothalamic tract, spinal trigeminal nucleus –> decrease pain and temperature sensation from CONTRA body and IPSI face
Sympathetic –> IPSI horner syndrome
Inferior cerebellar peduncle –> IPSI ataxia, dysmetria
Lateral medullary syndrome (Wallenberg)
Nucleus ambiguus effects are specific to PICA lesions
Anterior inferior cerebellar A
Lateral pons
Facial nucleus –> paralysis of face, low lacrimation, salivation and taste in anterior 2/3 of tongue
Vestibular nuclei –> vomiting, vertigo, nystagmus
Spinothalamic tract, spinal trigeminal nucleus –> decrease pain and temperature from CONTRA body and IPSI face
Sympathetic –> IPSI Horners
Middle and inferior cerebellar peduncles –> IPSI ataxia, dysmetria
Labryinthine A –> IPSI sensorineural deafness, vertigo
Lateral pontine syndrome
facial nucleus effects are specific to AICA
Basilar A
Pons, medulla, lower midbrain –> if RAS spared consciousness is preserved
Corticospinal and corticobulbar tracts –> quadriplegia, loss of voluntary facial, mouth and tongue movement
Ocular CN nuclei, paramedian pontine reticular formation –> loss of horizontal eye movements
Posterior cerebral A
occipital lobe –> CONTRA hemianopia with macular sparing, alexia without agraphia
Central poststroke pain syndrome
Neuropathic pain due to thalamic lesions
initial paresthesias followed in weeks to months by allodynia and dysethesia on CONTRA side
Diffuse axonal injury
via traumatic shearing forces during rapid acceleration- deceleration of the brain
devastating neuro injury –> coma, persistent vegetative state
MRI= multiple lesions involving white matter tracts
Broca’s aphasia
Broca area in inferior frontal gyrus of frontal lobe
Patient appears frustrated insight intact
Wernicke’s aphasia
superior temporal gyrus of temporal lobe
Patients do not have insight
Word salad
Conduction aphasia
can be caused by damage to arcuate fasciculus
Global aphasia
Broca + Wernickes
Transcortical motor aphasia
affects frontal lobe around Broca’s are. Broca is spared
Transcortical sensory aphasia
affects temporal lobe around Wernickes, Wernicke’s is spared
Transcortical mixed
Broca and Wernickes areas and arcuate fasciculus remain intact, surrounding watershed areas affected
Saccular aneurysm
Bifurcation in circle of willis (Acom and ACA)
Assoicated with ADPKD, Ehlers Danles
Risk- age, HTN, smoking , AA
Silent until rupture –> subarachnoid hemorrhage –> focal neuro deficits
Berry aneurysm in A com
Compression bitemporal hemianopia –> visual acuity deficits
Rupture –> ischemia in ACA distribution –> CONTRA lower extremity hemiparesis, sensory deficits
Berry Aneurysm MCA
Rupture –> ischemia to MCA –> CONTRA upper extremity and lower facial hemiparesis, sensory deficits
Berry aneurysm Pcom
compression –> IPSI CN III palsy –> mydriasis, ptosis and down and out
Charcot Bouchard Microaneurysms
Associated with chronic HTN
affects small vessels (lenticulostriate)
cause hemorrhagic intraparenchymal strokes
Not visible in angiography
Partial Seizure
Simple- consciousness intact
complete- impaired consciousness
Epilepsy
disorder of recurrent, unprovoked seizures
Status epilepticus
continuous or recurring seizures that may result in brain injury
Generalized seizures
Absence- no postictal confusion, blank stare
myoclonic- quick, repetitive jerks
Tonic clonic- alternating stiffening and movement, postictal confusion, urinary incontinence, tongue biting
Tonic- stiffening
Atonic- drop seizures
Fever
cytokine activation during inflammation
<40C
febrile seizures
T(x) Acetaminophen or ibuprofen
Heat Stroke
inability of body to dissipate heat
>40C
CNS dysfunction, end organ damage, acute respiratory distress, rhabdomyolysis
T(x) rapid external cooling, rehydration and electrolyte correction
Cluster HA
unilateral 15 minutes - 3 hours repetitive excruciating periorbital pain with lacrimation and rhinorrhea Males T(x): sumatriptan, O2, verapamil
Migraine
unilateral
4-72 hours
pulsating pain with nausea, photophobia, phonophonia, +/- aura
T(x): NSAIS, triptans, dihydroergotamine
Tensino HA
bilateral >30 min constant steady band like pain No photophobia, phonophobia or aura T(x): analgesics, NSAIDs acetaminophen
Akathisia
restlessness and intense urge to move
neuroleptic use or side effect of parkinson treatment
Asterixis
extension of wrists causing flapping motion
hepatic encephalopathy, Wilson
Athetosis
slow, snake like writhing movements
basal ganglia
Huntington
Chorea
Sudden jerky purposeless movements
Basal Ganglia
Huntington and acute rheumatic fever
Dystonia
sustained involuntary muscle contraction
Writers cramp, blepharospasm, torticollis
T(x): BOTOX
Essential tremor
high frequency tremor with sustained posture worsened with movement or when anxious
familial
self medicated with alcohol
T(x): nonselective B blockers
Intention tremor
slow zigzag motion when pointing
cerebellar dysfunction
Resting tremor
Uncontrolled movement of distal appendages alleviated by intentional movement
substantia nigra
Parkinsons (pill rolling)
Hemiballismus
sudden, wide flailing of one side of the body
CONTRA subthalamic nucleus
Myoclonus
sudden brief uncontrolled muscle contraction
renal and liver failure
Restless leg syndrome
Worse at rest/ night
relieved by movement
iron deficiency, CKD
T(x) DA agonists
Parkinson Disease
Pill rolling, rigidity, akinesia, postural instability, shuffling gait, small handwriting
loss of HA neurons and lewy bodies (a synuclein)
Huntington Disease
AD CAG repeat in HTT gene (Chr 4)
20-50 years
chorea, atheosis, aggression, depression, dementia
Anticipation
Atrophy of caudate and putamen with ex vacuo venticulomegaly
high DA, low GABA, ACh
Neuronal death via NMDA-R binding and glutamate excitotox
Alzheimers
dementia in elderly
increased risk in Downs
low ACh
Altered ApoE, APP
widespread cortical atrophy (hippocampus), narrow wide gyri and wide sulci
Senile plaques with B amyloid core
Neurofibrillary tangles (tau), Hirano bodies(protein rods in hippocampus)
Frontotemporal dementia
Early changes in personality and behavior or aphasia
associated movement disorders
frontotemporal lobe degeneration
tau (+)
Lewy body dementia
visual hallucinations, dementia with fluctuating cognition/ alertness
REM sleep behavior disorder and parkinsonism
onset < 1 year apart
Intracellular Lewy bodies in CORTEX
Vascular dementia
multiple arterial infarcts or chronic ischemia
decline in cognitive ability with late onset memory impairment
MRI/ CT multiple cortical/ subcortical infarcts
Creutzfeldt- Jakob Disease
rapidly progressive dementia with myoclonus and ataxia
periodic sharp waves on EEG
spongiform cortex
prions
Idiopathic intracranial HTN
high ICP with no obvious findings
risk- female, tetracyclines, obese, high vit A, Danazol
Associated with cerebral venous sinus stenosis
HA, tinnitus, diplopia, no AMS
papilledema
Lumbar puncture –> HA relief
T(x) weight loss, acetazolamide
Communicating Hydrocephalus
low CSF absorption by arachnoid granulations –> high ICP, papilledema, herniation
Normal Pressure Hydrocephalus
elderly, idiopathic
CSP pressure elevated episodically
Expansion of ventricles distorts the fibers of the corona radiata –> urinary incontinence, gait apraxia, cognitive dysfunction
Reversible with CSP drainage via lumbar puncture
Noncommunicating Hydrocephalus
caused by structural blockage of CSF circulation within ventricular system
Ex vacuo ventriculomegalu
appearance of high CSF on imaging but due to low brain tissue and neuronal atrophy
Alzheimers, HIV, Pick, Huntington
ICP normal
Multiple sclerosis
Autoimmune inflammation of demyelination of CNS
Acute optic neuritis, brain stem/ cerebellar syndromes, pyramidal tract demyelination, spinal cord syndromes
symptoms exacerbate with increased body temp
Relapsing and remitting
Women 20-30
low vit D
High IgG and myelin basic protein in CSF, oligoclonal bands
Periventricular plaques, multiple white matter lesions disseminated in space and time
Osmotic Demyelination Syndrome
massive axonal demyelination in pontine white matter secondary to rapid osmotic changes (hyponatremia correction)
acute paralysis, dysarthria, dysphagia, diplopia, locked in syndrom
Acute inflammatory demyelinating polyradiculopathy
Guillain Barre
autoimmune condition that destroys schwann cells via inflammation and demyelination of motor fibers, sensory fibers and PNS
Symmetric ascending muscle weakness and depressed DTRs in lower extremities, facial paralysis and respiratory failure]high CSF protein with normal cell count
Plasmapheresis or IVIg
Acute disseminated encephalomyelitis
multifocal inflammation and demyelination after infection or vaccination
rapidly progressive multifocal neuro symptoms, AMS
Charcot Marie Tooth
hereditary motor and sensory neuropathy
defective production of proteins involved in the structure and function of PNS or myelin sheath
AD PMP22 gene duplication
associated with foot deformities, lower extremity weakness and sensory deficits
Progressive multifocal leukoencephalopathy
Demyelination of CNS via destruction of oligodendrocytes rapidly progressive, usually fatal involve parietal and occipital areas visual symptoms high risk associated with natalizumab
Sturge Weber
Anomaly of NCC derivatives
activating mutation of GNAQ
capillary vascular formation –> port wine stain, IPSI leptomeningeal angioma –> seizures, intellectual disability, early onset glaucoma
Neurofibromatosis 1
AD mutation of NF1 (Chr 17)
cafe au lait spots, intellectual disability, cutaneous neurofibromas, lisch nodules, optic gliomas, pheochromocytoma, seizures, neuro signs
Tuberous Sclerosis
AD mutation of TSC1 (Chr 9) TSC 2 (Chr16)
Hamartomas in CNS and skin, angiofibroma, mitral regurgitation, ash-leaf spots, cardiac rhabdomyoma, mental retardation, angiomyolipoma, seizure, shagreen patches
increased incidence of subependymal giant cell astrocytoma and ungal fibromas
Neurofibromatosis 2
AD mutation of NF2 (chr 22)
bilateral vestibular schwannoma, juvenile cataracts, meningiomas, ependmomas
von hippel landau
AD deletion of VHL (chr 3p)
hemangioblastoma in retina, brainstem, cerebellem, spine, angiomatosis, bilateral RCC, pheochromocytoma
Glioblastoma multiforme
Adult primary brain tumor
Grade IV astrocytoma
Cerebral hemisphere, can cross corpus callosum
GFAP +, pseudopallisading, hemorrhage and microvascular proliferation
oligodendeoglioma
Adult primary brain tumor slow growing frontal lobes calcifies fried egg cells. chicken wire capillary pattern
Meningioma
Adult primary brain tumor
benign
females
near surfaces of brain and parasagittal region
Arachnoid cell origin
spindle cells concentrically arranged in whorled pattern, psammoma bodies
Hemangioblastoma
Adult primary brain tumor
cerebellar
associated with VHL when with retinal angioma
Secondary polycythemia
blood vessel origin
closely arranged, thin walled capillaries with minimal intervening parenchyma
Pituitary adenoma
Adult primary brain tumor
silent or hormone producing
Bitemporal hemianopia
prolactinoma –> galatorrhea, amenorrhea, low bone density due to suppression of estrogen, low libido, infertility in men
T(x) DA agonists, transspenoidal resection
Schwannoma
Adult primary brain tumor Cerebellopontine angle CN 5, 7, 8 involved S 100 + biphasic dense hypercellular areas with spindle cells alternating with hypocellular myxoid areas
Pilocytic astrocytoma
Childhood primary brain tumor well circumscribed posterior fossa astrocyte origin GFAP+ rosenthal fibers (corkscrew)
Medulloblastoma
Childhood primary brain tumor
cerebellum
compress 4th ventricle –> noncommunicating hydrocephalus
Neuroectodermal tumor, Homer Wright rosettes, small blue cells
synaptophysin +
Ependymoma
Childhood primary brain tumor
4th ventricle –> hydrocephalus
Ependymal cell origin
Perviascular pseudorosettes, rod shaped blepharoplasts
Craniopharyngoima
Childhood primary brain tumor supratentorial tumor bitemporal hemianopia Remnants of Rathke pouch calcifications, cholesterol crystals found in fluid within tumor
Pinealoma
Childhood primary brain tumor
pineal gland
parinaud syndrome (vertical gaze palsy), obstructive hydrocephalus, precocious puberty in males
Cingulate herniation
under falx cerebri
compress ACA
Transtentorial herniation
causal displacement of brain stem –> rupture paramedial basilar artery –> Duret hemorrhages
FATAL
uncal transtentorial herniation
uncus is medial to temporal lobe
Early- IPSI blow pupil (CN3), CONTRA hemiparesis
Late- coma, Kernohan phenomenon
Cerebellar tonsillar herniation
into foramen magnum
coma and death when herniation compress brainstem
Spinal muscular atrophy
congenital degeneration of anterior horns
LMN ONLY, symmetric weakness
floppy baby, tongue fasciculations
AR SMN1 mutation
Amyotrophic lateral Sclerosis
UMN and LMN degeneration so sensory or bowel deficits SOD1 defect flaccid limb weakness, fasciculations, atrophy, bulbar palsy, spastic limp weakness, hyperreflexia, clonus, pseudobulbar palsy T(c) Rilouzole
Complete occlusion of anterior spinal A
spares dorsal columns and Lissauer tract
mid thoracic ASA territory is watershed area
Can be caused by aortic aneurysm repair
UMN deficit below lesion and LMN deficit at lesion, loss of pain and temperature sensation below lesion
Tabes dorsalis
Tertiary syphilis
Degeneration/ demyelination of dorsal columns and roots –> progressive sensory ataxia
+ Romberg and absent DTRs
Associated with Charcot joints, shooting pain, Argyll Robertson pupils.
Syringomyelia
syrinx expands and damages anterior white commissure of spinothalamic tract –> bilateral symmetric pain and temperature sensation in capelike distribution
Chiai 1 malformation
Vitamin B12 deficiency
Subacute combined degeneration –> demyelination of spinocerebellar tracts, lateral corticospinal tracts and dorsal columns
ataxic gait, paresthesia, impaired position/vibratory sense, UMN symptoms
Cauda equina
compression of spinal roots L2 and below via intervertebral disc herniation or tumor
radicular pain, absent knee and ankle reflexes, loss of bladder and anal sphincter control, saddle anesthesia
Poliomyelitis
Polio replicate in oropharynx and small intestine before spreading via blood stream to CNS
Causes destruction of cells in anterior horn (LMN)
asymmetric weakness, hypotonia, flaccid paralysis, fasciculations, hyporeflexia, muscle atrophy, respiratory failure
CSF high WBC, slight high protein
Brown Sequard
Hemisection of spinal cord
IPSI loss of all sensation at level of lesion
IPSI LMN signs at level of lesion
IPSI UMN signs below level of lesion
IPSI loss of proprioception, vibration, light and tactile sense below level of lesion
CONTRA loss of pain, temperature and crude touch below level of lesion
Friedrich Ataxia
AR GAA repeat on Chr 9
impaired mitochondrial functioning
Degeneration of lateral corticospinal tract, spinocerebellar tract, dorsal column and DRG
staggering gait, frequent falling, nystagmus, dysarthria, pes cavus, hammer toes, DM, hypertrophic cardiomyopathy
CN V motor lesion
jaw deviates toward side of lesion due to unopposed force from the opposite pterygoid M
CN X motor lesion
uvula deviates away from the side of lesion
weak side collapses
CN XI lesion
weakness in turning head to CONTRA side. Shoulder droop on side of lesions
CNXII motor lesion
LMN lesion
tongue deviates toward side of lesion
Bell Palsy
Post HSV reactivation, lyme disease, herpes zoster, sarcoidosis, tumors, DM
T(x) corticosteroids and acyclovir
UMN lesion facial N
at motor cortex, connection from motor cortex to facial nucleus in pons
CONTRA
lower muscles of facial expression
forebrain is spared
LMN lesion Facial N
facial nucleus CNVII
IPSI
upper and lower muscles of facial expression
forebrain affected
incomplete eye closure, hyperacusis, loss of taste sensation to anterior tongue
Outer ear
visible portion of ear (pinna)
auditory canal and tympani membrane
Transfer sound waves via vibration of tympanic membrane
Middle ear
air filled with bones (malleus, incus, stapes)
ossicles conduct and amplify sound from tympanic membrane of inner ear
Inner ear
snail shaped, fluid filled cochlea
contain basilar membrane that vibrates secondary to sound waves
vibration transduced via hair cells –> auditory N signaling –> brainstem
Low frequency
heard at apex near helicotrema
High frequency
heard at base of cochlea
Weber test
Normal: no localization
Conductive: localizes to affected ear, low transmission of background noise
Sensorineural: localized to unaffected ear, low transmission of all sound
Rinne test
AC > BC = normal
BC > AC = conductive
AC > BC = sensorineural
Noise induced hearing loss
damage to stereociliated cells in organ of Corti
loss of high frequency hearing first
sudden extremely loud noises can produce hearing loss due to typanic membrane rupture
Presbycusis
age related progressive bilateral/ symmetric sensorineural hearing loss due to destruction of hair cells at the cochlear base
Cholesteatoma
overgrowth of desquamated keratin debris within the middle ear space
may erode ossicles, mastoid air cells. –> conductive hearing loss
painless otorrhea
Peripheral vertigo
inner ear etiology
Meniere, vestibular N infection, BPPV
T(x) antihistamines, anticholinergic, antiemetics, low salt diet
Central vertigo
Brainstem or cerebellar lesions
stroke, demyelinating disease, posterior fossa tumor
directional or purely vertical nystagmus, skew deviation, diplopia, dysmetria
Conjunctivitis
inflammation of conjunctiva
Allergic- itchy bilaterally
Bacterial- pus treat with Abx
Viral (most common)- adenovirus, sparse mucous discharge, swollen preauricular node, increased lacrimation, self resolving
Hyperopia
farsightedness
eye too short for rereactive power of cornea and lens –> light focused behind retina
correct with convex lens
Myopia
nearsightedness
eye too long for refractive power of cornea and lens –> light focused in from of reina
correct with concave lens
Astigmatism
abnormal curvature of cornea –> different refractive power at different axes
correct with cylindrical lens
Presbyopia
age related impaired accommodation due to decreased lens elasticity, changes in lens curvature, decrease strength of the ciliary M
need reading glasses
Cataracts
painless, bilateral opacification of lens –> glare and decrease vision
old age, smoking, alcohol, sunlight, corticosteroid use, DM, trauma, infection
Congenital- galactosemia, galatokinase deficiency, Trisomies, TORCH, Marfan, Alport, myotonic dystrophy, NF2
Aqueous humor pathway
produced by nonpigmented epithelium on ciliary body –> trabecular outflow –> canal of schlemm –> episcleral vasculature
or
Uvesleral outflow –> uvea or sclera
Glaucoma
optic disc atrophy with characteristic cupping
elevated IOP and progressive visual field loss if untreated
open angle glaucoma
old age, AA, FHx
painless
Primary- unclear
Secondary- blocked trabeculae meshwork from WBCs, RBCs, retinal elements
Closed angle glaucoma
Primary- enlargement or anterior movement of lens against central iris –> obstruct normal aqueous flow –> fluid buildup behind iris
Secondary- hypoxia from retinal disease induces vasoproliferation
Chronic: asymptomatic with damage to optic N and peripheral vision
Acute: emergency, high IOP pushes iris forward. Painful, red eye, sudden vision loss, halos around lights, frontal HA
Uveitis
inflammation of uvea
anterior- iritis
posterior- choriditis, retinitis
systemic inflammatory disorders
Age related macular degeneration
distortion and eventual loss of central vision
Dry: deposition of yellowish extracellular material. gradual loss of vision. Prevent progression with multivitamin and antioxidants
Wet: rapid los of vision due to bleeding secondary to choroidal neovascularization. Treat with anti VEGF injections
Diabetic retinopathy
Retinal damage due to chronic hyperglycemia
Nonproliferative: damages capillaries leak blood –> lipids and fluids seep into retina –> hemorrhage and macular edema
Proliferative: chronic hypoxia –> new blood vessel formation –> traction on retina –> retinal detachment
Hypertensive retinopathy
flame shaped retinal hemorrhages, arteriovenous nicking, microaneurysms, macular star, cotton wool spots
papilledema
Retinal V acclusion
blockage of central or branch retinal V due to compression from nearby arterial atherosclerosis
Retinal hemorrhage and venous engorgement
Retinal detachment
separation of neurosensory layer of retina from outermost pigmented epithelium –> degeneration of photoreceptors –> vision loss
crinkling retinal tissue
Central retinal A occlusion
acute, painless, monocular vision loss
retina cloudy with attenuated vessels and cherry red spot of fovea
Retinitis pigmentosa
inherited progressive retinal degeneration
Nyctalopia –> peripheral vision loss
bone spicule shaped depositis
Papilledema
optic disc swelling due to increased ICP
enlarged blind spot and elevated optic disc with blurred margins
Leukocoria
loss of red reflex
retinoblastoma, congenital cataract, toxocariasis
Miosis
constriction, PNS
Edwinger-Westphal nucleus to ciliary ganglion via CN III
short ciliary N to sphincter pupillae muscles
Pupillary light reflex
light in either retina sends a signal via CN II to pretectal nuclei in midbrain that activates bilateral edinger westphal nuclei
pupils constrict bilaterally
Mydriasis
dilation, SNS
hypothalamus to ciliospinal center of Budge C8-T2
exit T1 to superior cervical ganglion
plexus along internal carotid through cavernous sinus, enters orbit as long ciliary nerve to pupillary dilator muscles
Marcus Gunn pupil
when light shines into a normal eye constriction of the ipsilateral and contralateral eye is observed
when light is sprung to the affected eye, both pupils dilate instead of constrict due to impaired conduction of light signal along the injured optic N
optic neuritis, early MS
Horner Syndrome
SNS problem in face
Ptosis, anhidrosis, miosis
pontine hemorrhage, lateral medullary syndrome, spinal cord lesion above T1, stellate ganglion compression, carotid dissection
Ocular motility
CN 6- Lateral rectus
CN 4- Superior oblique
CN3- everything else
CN3 palsy
ischemia, uncal herniation, Pcom aneurysm, cavernous sinus thrombosis, midbrain stroke
Motor output to extraocular muscles –> ptosis, down and out
PNS output–> diminished or absent pupillary light reflex, blown pupil, down and out
CN 4 palsy
pupil is higher in the affected eye
head tilt to contralateral/ unaffected side to compensate for lack of intorsion in affected eye
Cn 6 palsy
affected eye unable to abduct and is displaced medially in primary position of gaze
Cavernous sinus syndrome
presents with variable ophthalamoplegia, decreased corneal sensation, Horner syndrome and occasional decreased maxillary sensation
secondary to pituitary tumor mass effect, carotid cavernous fistula, or cavernous sinus thrombosis
Internuclear ophthalmoplegia
medial longitudinal fasciculus- crosstalk between CN 6 and CN3. coordinate both eyes to move in same horizontal direction.
Lesion- INO, horizontal gaze palsy. abducting eye has nystagmus. convergence normal
Barbiturates
barbital
GABAa action decrease via increased duration of Cl- channel
used for sedation for anxiety, seizures, insomnia, anesthesia
Adverse: respiratory and CV depression, dependence, drug interactions.
Contra in porphyria
Benzos
-pam
GABAa, increase frequency of Cl- channel opening, decrease REM
used for anxiety, pain, spasticity, status elipticus, eclampsia, detox, night terrors, sleepwalking, anesthetic, insomnia
Adverse: dependence
T(x) OD with flumazenil
Nonbenzo hypnotics
zolpidem, zaleplon, eszopiclone
act via BZ. Reversed by flumazenil
used for insomnia
adverse: ataxia, HA, short duration
Suvorexant
orexin antag
used for insomnia
Adverse: CNS depression, HA, abnormal sleep related activities
Contra: narcolepsy, with CYP3A4 inhibitors
Ramelteon
melatonin receptor agonist. bind MT1 and 2 in SCN
used for insomnia
aderse: dizzy, nausea, fatigue, HA
Triptan
5HT agonist. Inhibit trigeminal N activation, prevent vasoactive peptide release induce vasoconstriction
used for acute migraine, cluster HA
adverse: coronary vasospasm, mild paresthesia, serotonin syndrome
Parkinson Disease Therapy
Bromocriptine, Amantadine, Levodopa, Selegiline, Antimuscarinics
DA agonists
Bromocriptine- Ergot
Non-ergot- pramipexole, ropinirole (tox= nausea, impulse control disorder, postural hypotension, hallucinations, confusion)
Increase DA availability
Amantadine
increase DA release and decrease DA reuptake
Tox- peripheral edema, livedo reticularis, ataxia
Increase L DOPA availability
Levodopa/ carbidopa- carbidopa block peripheral conversion of L DOPA to DA by inhibiting DOPA decarboxylase. Reduce side effects of peripheral L DOPA conversion into DA
Entacapone and tolcapone prevent peripheral L DOPA degradation to 3-OMD by inhibiting COMT (use with levodopa)
Prevent DA breakdown
selegiline, rasagiline- block conversion of DA to DOPAC by inhibiting MAO
Tolcapone- crosses BBB and blocks conversion of DA to 3 MT in the brain by inhibiting COMT
Curb excess cholinergic activity
Benzotropine, trihexylphenidyl
improve tremor and rigidity but has little effect on bradykinesia in Parkinson
Carbidopa/ Levodopa
increase DA in brain. L DOPA can cross BBB and is converted by DOPA decarboxylase to DA. Carbidopa is peripheral and given with L DOPA to increase bioavailability
used for parkinson
Adverse: nausea, hallucination, postural hypotension. on off phenomenon
Selegiline and rasagiline
selective inhibit MAO B –> increase DA availability
use for adjunctive agent to L DOPA in parkinsons
adverse: may enhance adverse effects of L DOPA
Alzheimer Therapy
AChE inhibitor (Doneprezil, rivastignmine, galantamine)- first line, adverse is nausea, dizziness and insomnia NMDA antagonist (Memantine)- moderate to advanced dementia, adverse is dizzy, confusion, hallucinations
ALS treatment
riluzole
decrease neuron glutamate excitotoxicity
Huntington Treatment
tetrabenazine
inhibit VMAT –> decrease DA
chorea and tardive dyskinesia
Anesthetics general
must be lipid soluble to cross BBB
decrease solubility in blood –> rapid induction and recovery
Increase solubility in lipids –> increased potency –> lower MAC
Inhaled anesthetics
-ane, N2O
myocardial depression, respiratory depression, post op nausea and vomiting, increased cerebral blood flow, decreased cerebral metabolic demand
Adverse: hepatotox, nephrotox, proconvulsant, expansion of trapped gas in body
Malignant hyperthermia
lige threatening condition in which inhaled anesthetics or succinylcholine induce severe muscle contractions and hyperthermia.
AD mutation in RYR1 gene
Treat with Dantrolene
Thiopental
IV anesthetic
facilitate GABAa
used for anesthesia induction, short surgery
high lipid solubility
Midazolam
IV anesthetic
facilitate GABAa
procedural sedation, anesthesia
cause post op respiratory depression, low BP, anterograde amnesia
Propofol
IV anesthetic
potentiate GABAa
rapid anesthesia induction, short procedures
cause respiratory depression, hypotension
Ketamine
IV anesthetic
NMDA antagonist
dissociative anesthesia, sympathomimetic
increase cerebral blood flow, disorientation, hallucination, vivid dream
Local anesthetics
esters= -caine amides= have two I’s
block Na+ channels by binding receptors
enhanced when given with vasoconstrictors
used in minor surgical procedures, spinal anesthesia
adverse: CNS excitation, CV tox, hypertension, hypotension, arrhythmias, methemoglobinemia
Depolarizing NMJ block
succinylcholine- strong AChR agonist –> sustained depolarization and prevent muscle contraction
reversal of blockade via AChE inhibitor
Complications- hypercalcemia, hyperkalemia, malignant hyperthermia
Nondepolarizing NMJ block
-cur-
competitive ACh antagonist
reversal of blockade via AChE inhibitors with anticholinergics to prevent muscarinic effects
Baclofen
GABAb receptor agonist in spinal cord
use for muscle spasticity, dystonia, MS
cyclobenzaprine
Brainstem
use for muscle spasticity
Dantrolene
prevent Ca2+ release from SR of skeletal M by inhibiting RyR
used in malignant hyperthermia and neuroleptic malignant syndrome
Tizanidine
a2 agonist for CNS
used in muscle spasticity, MS, ALS, cerebral palsy
Opioid analgesics
close presynaptic Ca2+ channels, open postsynaptic K+ channels –> decrease synaptic transmission
inhibit release of ACh, NE, 5HT, glutamate, substance P
used in moderate to severe pain, diarrhea, acute pulmonary edema, maintenance programs for heroin addicts
Adverse: nausea, vomiting, pruritis, addiction, respiratory depression, constipation, sphincter of Oddi spasm, miosis
Treat tox with naloxone
Pentazocine
K opioid receptor agonist and mu opioid receptor antagonist
used for analgesia for moderate/severe pain
Butorphanol
K opioid agonist and mu opioid partial agonist
used in severe pain
Tramadol
weak opioid agonist, NE and 5HT reuptake inhibitor
used in chronic pain
decrease seizure threshold, serotonin syndrome
B blockers in glaucoma
timolol, betaxolol, cartelol
decrease aqueous humor synthesis
adverse- no pupillary or vision changes
a agonists in glaucoma
epi, apraclonidine, brimonidine
decrease aqueous humor synthesis
adverse: mydriasis, blurry vision, ocular hyperemia, foreign body sensation, allergy, pruritis
Diuretics in glaucoma
acetazolamide
decrease aqueous humor synthesis via carbonic anhydrase inhibition
adverse- no pupillary or vision changes
Prostaglandins in glaucoma
Bimatoprost, Iatanoprost
increase outflow of aqeous humor
Adverse: darken color of iris, eyelash growth
Cholinomimetics M3 in glaucoma
Direct- pilocarpine, carbachol
indirect- physostigmine, echothiopate
increase outflow of aqueous humor
adverse: miosis and cyclospasm
