Cerebellum and basal gangliaBasal- accessory system, mainly working with cortex for complex movement (writing) Scale

and timing- how fast and big to write; posterior parietal cortex spatial coordinates for motor control and proprioception Caudate nucleus, putamen, globus pallidus, substantia nigra, subthalmic nucleus (basically everything arouns the thalamus) Internal capsule (caudate/putamen) Signal from cortex (premotor, prefrontal, very little primary and somatosensory) travels to putamen then globus pallidus then ventral thalamus/subthalmus abck to cortex Globis pallidus lesions spontaneous writhing of arm neck face (athetosis); subthalmus flaling limbs (hemiballismus); putamen flicking motions (chorea); substantia nigra (parkinsons- rigidity, akinesia, tremors) Globis pallidus (needs to be inhibited for movement and activation of thalamus) Putamen direct pathway stimulation enables movement (glutamate from cortex) indirect pathway stimulation inhibits movement (dopa from substantia nigra inhibits this inhibition) Caudate major role in cognitive motion, receive info from association areas; to globis pallidus then thalamus then cortex (not primary); subconscious thought for movement responses to thoughts Gaba from cortex to ganglia to nigra back to cortex makes neg feedback loop= stabilization Parkinsons-paralysis agitans, substantia nigrans damage (pars compacta) (less d1 stimulation and no d2 inhibition (no longer stopping the brakes) so movement is inhibited), this prevents the dopamine signals to inhibit extra movement; rigidity, tremor at rest (involuntary, feedback oscillation due to high feedback gain after loss of inhibition), hard to initiate movement since all muscles are contracted due to nonstop stimulus from corticospinal pathway (need extreme concentration to move, could be dopamine loss in limbic system); l-dopa helps treat symptoms of rigidity and akinesia; ldeprynl inhibits monoamine oxidase (dopa cutter)and destruction of substantia nigra; aborted brains producing dopamine last a few months; surgery to give lesions and reduce feedback Huntingtons- hereditary; flicking movementsdistortional and severe dementia; not loss of gaba in caudate and putamen but ach in cortex; spontaneous outbursts of movement signals; cag codon in huntingtin Hindbrain- general control, axial tone Cerebellum- smooth out equilibrium, stretch reflex for heavy loads; next movement (juking then cutting) Ant- tone; post coordination; vestibule/flocculonodular posture balance Superior peduncle- - major output Molecular layer- outer, parralel Deep nuclei- signal comes in goes to deep and to cortex so cortex sends inhibitory signal one second later Vermis/fastigial medulla, equilibrium, posture Intermediate/interposedthalmus and cortex then brain stem; distal/peripheral motion Cerebellar cortex/lateral/dentate coordinate sequential Climbing fibers give action potential big spike with little ones; movement output (errors), purkinje cells; inhibitory output GABA to cerebellum and vestibular nuclei; controls output of cerebellum Many mossy fibers to stimulate single simple spike; somatosenroy equilibriyum, spinal cord, pontine; granule Purkinje and deep nuclear cells fire constantly

Deep nuclear slightly constant stimulated as outweighs inhibition Basket and stellate inhibit purkinje Dorsal sensory, anterior feedback on actual movement Granule cell- input of mossy combine; excite purkinje, basket, stellate, golgi Cerebrocerebellum (pontocerebellum)- image of motion Intention, dysdiadochkinesia, dysmetria hypotonia Spino cerebellum- control coordination Gait ataxia posterior- trunk muscles medulloblastomas; anterior- lower limbs lamnutrition Vestibulocerebellum- equilibrium; semicircular ducts, flocculo gets visual input Flocculonodular syndrome- truncal atacia; no heel toe talking Hypotonia- loss of resistance, floppy Disequilibrium- gait trunk dystaxia Dyssynergia- no coordination Dysarthria-speech Dystaxia-voluntary Dysmetria-cant stop Intention tremor; dysdiadochokinesia (no alternation) Nystagmus-dystaxia of eyes Decomposition Mollarets triangle ( red nucleus, inferior olive, dentate nucleus) lesion = palatal myoclonus Astrocytoma- children; surgical Medulloblastoma- children, vermis; granular layer; hydrocephalus; Ependymomas-children; spinal cord, fourth ventricle Friedrich ataxia- recessive; chronic myocarditis (presents like no b12) Cerebello olivary degeneration (holmes)- auto dom; no purkinje or neurons in olivary nuclei; gait , dysarthria, intention Olivopontocerebellar- auto dominant; demyelination; Parkinson signs, gait ataxia

Hearing Membrane- malleus, incus stapes, cochlea membranous labyrintyh at oval window Reduce stapes amplitude but increase force (22X) Loud sounds contract tensor tympani and stapedius muscle, reduce conduction, increased rigidity; attenuation reflex reduces intensity of lower frequency sounds (protects, and helps drown out background noise); also reduces hearing your own voice Chochlea- scala vestibuli, (reissners/vestibular membrane, so thin almost nonexistent) scala media,(basilar membrane with organ of corti) scala tympani Basilar membrane has fibers that get longer and thinner (low frequency) Tension of fibers moving towards round window as oval is puished creates wave; to dissipate energy Separate high frequencies by transmitting enough into the cochlea to have the opportunity to spread out and dissipate at right spot Organ or corti on basilar membrane and fibers Single row internal 3-4 rows of external Most ganglions on inner hair cells, spiral ganglion connect to cochlear nerve

Stereocilia project onto tectorial membrane; can be depolarized (bend toward vestibule)or hyperpolarized; by reticular lamina motion moving from basilar membrane Outer hair cells tune Tips are in super positive endolymph making them more sensitive Below 200-20 cause volleys that create pattern you can detect Louder sounds- increase amplitude so increase nerve rates; more hair cells to react; outer hair cells to stimulate Compression of intensity lets us hear over a range Corti- dorsal and ventral cochlear nuclei; synapse then opposite superior olivary nucleus lateral leminiscus00> inferior colliculus medial geniculate lemnisuc auditory radiation and cortex in temoporal lobe superior gyri Most sound goes to contralateral brain;p Multiple crossovers (trapezoid body; lateral lemnisci, commissure of inferior colliculi Direct innervation or reticular activating system in brain stem to react to loud noises Collateral fibers into cerebellum Less synchronization with frequency as you progress through path Primary and secondary cerebral auditory cortex Low frequency anterior; multiple tonotropic maps (location, pitch, types) Lateral inhibition help to focus sound to specific areas of brain Regions detect patterns of sound Destruction of areas causes minor deafness but crossovers reduce, mainly processing and localization; association area damamge cant get meaning of music (wernickes) Intensity (higher frequencies) and time lag (below 3000) localize sound distance; pinnae localize direction (by quality) Begins in superior olivary system (lateral is direction; medial measuires time lag) Nerve deafness- damage to nerve or cochlea; audiometer negative for air and bone Conduction deafness- tympanium ossicular system has been destroyed or ankylosed waves can be condueced by generator; totally ankylosed stapes can be replaced Middle ear fibrosis due to repeated infection (otosclerosis) normal bone conduction

Vestibular Membranouse labyrinth cochlea, semicircular canals, utricle and saccule Macula- orientation of head compared to gravity utricle (horizontal, for upright determinantion) saccule (vertical laying down orientation) Hair cells synapse sending signals of stataconia bending hair cells Stereocilia and kinocilum bend opening channels for ions (towards kino depolar); continuous signals that increase or decrease; pattern from different directions (upside of slope increase firing) Sudden acceleration- lean forward til hairs aint moving Semicircular ducts all right angles to each other; ampulla filled with endolymph Crista ampullaris with cupula (bends in response to fluid staying still with inertia); hair cells detect bending and send signals by vestibular nerve when rotating head; left turn causes left canal flow with excitation and right canal inhibition Extended rotation endolymph still, signal attenuates (elastic recoil of ampulla); stop rotation endolymph moves, cupula bends Predict disequilibrium

Send signals to eyes through vestibular nuclei medial laongitudinal fasiculus to oculomotor for eye movmenet with and against rotations Vestibualr nuiclei in brain stem receives body and neck signals for head relationship Neck inhibits signals when bent back Foot pressure pads signal balance Receive infor from ocular, eyes closed with vestibular damage cant move Eyes move opposite a turn slowly then spring with the turn (nystagmus is in direction of turn and fast phase) Cold water- nystagmus to opposite side (look slowly then quickly away); intact unconscious slow to water; bilateral mlf lesion just one eye to water; low brainstem no response) Vestibular nerve nuclei at medullar, cerebellum, reticular nuceli Flocconudular gets from semicircular; equivalent to losing

EYE Retina- part of the brain, transforms light into electricity Cornea, Iris, lens, retina anterior chamber Fovea gaze point Photoreceptors (rods and cones) 1st order; synapse with bipolar synapse ganglion which form optic Outerplexiform layer horizontal cells connect receptos Inner plexiform amarcine cells connect ganglions More rods (low light, seeing in the dark) Cones (bright light, sharp vision and color) Both have outer segments of flat disks with pigment Inner segment (organelles) that synapse with bipolar cells Photons absorbed turned into signals Rods have rhodopsin (g protein linked)__> metarhodopsin scotopsin retinene; activates transfucin which cleaves GMP; this closes sodium channels which hyperpolarizes in light; less transmitters on bipolars and new signal Cones respond to blue green red; when hit with color they also close sodium channels and hyperpolarize Bipolar cells get signals from dozens of receptors; these can be tuned by horizontal cells which are attached to both and can sharpen bipolar cell; respond to little specks of light (on center and off center) Amarcine cells synapse with multiple bipolars and ganglions to sharpen image more and create on off center regions Central vision in macula; with pit of fovea full of cones Magnocellular ganglion with larger diameter for motion but not details Parvocellular with thinner axons for form and color Join on lateral geniculate nucleus Ganglion cells form nerve fiber layer; forming optic nerve at optic disk (blind spot) Pupillary reflex constricts in bright light Gmp levels increase in light, leaving channels open and desensitizing to light Mix of colors makes white light Intensity of color perception = to frequency of impulse Color blindness- weakness of absence of cone (usually red green confusion) Lens held by capsule and ciliary body, usually tight with lens flat, when accommodating they loosen and lens become biconvex

Eye naturally set for distant objects; to see close must increase refraction and accommodation (more biconvex); lose ability with age Hyperopia focal point is behnd eye or eye is too short (curved lens infront fixes) Myopia (near sighted) focal poin in front or eye is too long (biconcave lens) or get closer Astigmatism- curvature of lens or cornea is greater in one axis Scotomas- blind spot; central (macular in optic or retrobulbar neuritis; central acuity impaired); centrocecal (point of fixation to blind spot) annular (encircle point) scintillating (bright lights in line of vision; aura before migraine) Retrobulbar neuritis- MS, no fundus changes so far back on nerve Pailledema- choked disk, ICP increased, brain tumor; 24-48 hours, big blind spot no other changes, unless optic atrophy Optic atrophy- decreased visual acuity; change in of the optic disk to pink/white/gray; primary nerve, seoncdayr papillaedema Holmes alde- tonic pupillary reaction, no tendon reflexes, slow contraction and dilation to light and darkness Single eye (eye, retina, nerve) Field defects in both eyes (chiasm, racts, cortex) Chiasm bitemporal hemianopsia lateral visual blindness as nasal fibers are injured; Behind chaism- temporal one side and nasal othe, homonymous hemianopsia; field defect opposite lesion Temporal lobe lesions affect Meyers and upper field contralateral (pie in the sky) superior quadrantanopsia End of nerve before cortex- macular sparing; half a field opposite lesion Endstage glaucoma- leaves macula seeing Upper altitudinal heiamopia; destroy lingual gyri all upper vision lost Cunei- lower vision lost; upper part of tract Optic nerve Lamina cribosa in sclera; 1 million fibers; goes through cnal to chiasm; nasal side crosses; lateral ipsilateral; both of them see the opposite field of vision so right brain gets left field etc; Tract to lateral geniculate body and superior colloculus Geniculate bodies in thalamus; layers correspond to different fiber types (parvo. Magno) from different sides Proceed ipsilateral to optic radiation (geniculocalcarine fibers) to calcarine cortex in occipital lobe Meyers loop upper visual field, lower tract Superior colliculs projects to spinal cord, controlling reflexes Parasympathetic neurons to edingerwestphal nucleus to ciliary ganglia; these act on sphincter muscles of iris for pupillary reflex (this is bilateral and results in consensual and direct response) Visual cortex Multiple areas in temporal, occipital, parietal lobes Primary gets blood from calcarine branch of posterior cerebral; above and below calcarine fissure (middle is macula, up to bottom clockwise) Striate because of myelination on stain; blobs get colors; interblobs get shap; magno (motion, depth, form) goes ddep MT on superior temporal sulcus- localization Macula ismagnified within topotropic maps Simple cells have on /off centers; respond to stimuli at one locations orientation;

Complex cells- larger receptions; look for certain stimuli but anywhere in visual field; some receive info from both eyes; many prefer one eye (ocular dominance) arranged to alternate and combine images Orientation columns have simple and complex cells Pupillary dilation- sympathetic; lesions cause ipsilateral horners; neurons from hypothalamus go to ciliospinal center; ciliospinal center of budge; superior carvial ganglion goes to dilator of iris Marcus gunn pupil- no direct response to trigger a consensual in one eye (has consensual when other eye stimulated) Horners- eye lid closed, pupil constricted; cervical sympathetic interruption; dilation of blood vessels (red) and impossible to sweat on that side (central no sweating on body that side, cervical is upper body, after bifurcation sweating not affected); caused by lesions or brainstem infarction; oculosympathetic

pathway involved in Horner's syndrome. from the hypothalamus to the intermediolateral column of the spinal cord, then to the superior cervical (sympathetic) ganglion, and finally to the pupil, smooth muscle of the eyelid, and sweat glands of the forehead and face; unilateral; birth horners could see blue eyes
Internuclear ophthalmoplegia- eye can look lateral but not nasal unless you are crossing your eyes; medial longtitudinal fasiculus; from abducens to contralateral oculomotor; abducens and oculomotor are uncoupled; MS or intrinsic brainstem disease; older patients vascular One and half palsy- medial longitudinal fasiculus and ipsilateral paramedian; inter plus inability to gaze towards lesion; one eye is stuck and the other can go from lateral to midpoint and thats it; You cant go past midpoint towards lesion, only one eye can look away from lesions; pontine hemorrhage, ischemia, infections, MS Cn3 palsy- eye deviates lateral/down when looking straight ahead; eyelid can also be closed; double vision unless looking at where fucked up eye goes naturally; parasympathetic affected (dilated fixed pupil; cycloplegia); transtentorial herniation (tumor forces hippocampus through tentorial notch, compresses nerve (parasympathetic affected first); motor damaged by diabetes Cn6 palsy- eye stays forward when looking to side; deviates nasaly Gaze palsy- paired muscles dont work; supranuclear lesion; affecting both eyes Parinaud syndrome- cant look up or cross Fourth nerve palsy- cant move eye down when its nasal; elevated during primary gaze and more so during adduction (nasal) can be corrected by tilting head away from fucked up eye; tilt towards makes it worse Arygyll Robertson pupil- dont react to light; prostitute pupil; still constrict when focus Comatose eye- cows Non intact brainstem- dolls eyes move with head Brodmans 8- coluntary eye movements Stimulate by lesions; contralateral deviation away from lesion Destruction; ipsilateral deviation to wards lesion Eye movementCN3 innvervates everything but superior oblique and lateral rectus Includes edinger westphal nucleus Levator palpebrae superioris (eyelid open; closed by cn vii orbicular muscle), superior (elevate), medial (adduct), inferior rectus (depres); inferior oblique (elevate); somatic Ciliary and constrictor pupillae Cn4- crosses inside midbrain; superior oblique (depress and abduct eye); head tilt to compensate Cn6- lateral rectus muscle (abduct); long nerve that is susceptible to compression from fossae;

Common muscle palsycant abduct the eye because medial rectus Scan in saccades (when moving in a car jump from focal point to focal point) suppression of jump ; happens during reading and observing art smooth pursuit tracks- cortical mechanism detects movement and copies the eyes to it; superior colliculi allow for sudden turning to disturbance (topographic map); go through medial longitudinal fasiculus so body and neck turn keep objects in focus for two eyes by using multiple pairs of fibers for various distances Eyes move in conjuction but use different muscles (conjugate gaze) Lateral gaze in paramedian pontine reticular by abducens; activated by head movement Eye movement to right signals fight abducens nucleus which connects to left oculomotor nucleus (this connection is medial longitudinal fasciculus) to move left eye nasal Vertical- oculomotor and trochlear; connect in rostal interstitial nucleus; everything in midbrain Vergence- center in pretectum; includes somatomotor oculomotor nucleus; edinger westphal nucles Interconnection among brainstem with medial longitudinal fasiculus; reciprocal innervation to relax and contract in sync Premotor allows you to find something to focus on; secondary visual in occipital allows you to lock on Involuntary locking- continuous tremor by continuous motor contraction; slow eyeball drift; sudden flicking back to center of fovea( these help make the object strike cones in the fovea); need superior colliculi Cn 3 paralysis- trantentorial herniation; diplopia; drooping eyelid; you look down and out (CN 4 and 6 unoppossed) dilated pupil, no accommodation Transterntorial herniation- compresses; no constriction, strabismus Aneurysms- compress Diabetes- oculomotor palsy; spares constriction CRANIAL NERVES Olfactory, optic oculomotor trochlear trigeminal abducen facial vestibulocochlear glossopharyngeal vagus accessory hypoglossal Special senses- olfaction, seeing, taste (7,9,10) hearing balance Touch pain temp- 5,7,9,10 Branchiomotor 5,7,9 (throat and neck, face) Visceromotor 3 (ciliary ganglion and edinger westphal),7 (salivary except parotid),9 (parotid gland),10 (organs from esophagus to left colic flexure); then sphlancic para nerves; 1st in CN and then to organ Somatomotor 3,4,6, 11, 12 CN1 olfactory- smelling; cribiform plate contains receptors which conjugate on mitral and granule cells; commissure> stria>tract>bulb>cribiform; continuously renewed Unmyelinated; directly to telencephalon/forebrain; anosmia CN2 optic- ganglions combine make nerve> optic canal> chiasm>tract>lateral geniculate nucleus on thalamus> Meyers loop and radiations> visual cortex Eye sees things upside down, blurry and reversed CN3 oculomotor- external eye muscles except lateralis and superior oblique; sphinter, pupillae, ciliary (accommodation from edinger westphal then ciliary ganglion); passes from interpeduncular fossa of midbrain, cavernous sinus through orbital fissure Ciliary muscles relax, pulls ligaments lens flattens can see far; to see near ciliary muscles contract, ligaments felax lens becomes convex Proximity to basilar bifurcation, means aneurysm may impinge on foot of cn3 in interpenducular fossa

Cn4 trochlear- superior oblique; mesencephalic trochlear nucleus exit posterior then cross and loop around the back; passes through superior orbital fissure; head tilting if paralyzed to correct visison Cn5 trigeminal- 3 branches of sensory and motor; ophthalmic, maxillary, mandibular; 1st pharyngeal arch; mastication and sensory for face Trigeminal neuralgia- probably compression, or blood vessel pressing/irritating nerve; extreme facial pain at lightest stimulus Ophthalmic- superior orbital fissure> frontal (forehead), lacrimal (lacrimal, lateral eye) nacociliary (eyeball and nose) Maxillary- foramen rotundum> pterygopalatine> inferior orbital fissure> infraorbital (eyelid) superior alveoloar (maxilla, sinus and teeth) pterygopalatin (palate) zygomatic (superior cheek) Mandibular- foramen ovale> infratemporal> auriculotemporal (ear, temple); buccal (inferior cheek); inferior alveolar (mandible and teeth) lingual (anterior tongue) masticatory; mastication (masseter, temporalis, pterygoid, mylohyoid) Sensory are crossed and report to other side of brain; motor are both crossed and uncrossed Lesions- loss of facial sensation; corneal reflex; cant chew; deviated jaw; tensor tympani paralysis and partial deafness Cn6 abducens- lateral rectus muscle; superior orbital fissure and cavernous sinus

Facial nerve- 2nd pharyngeal arch, salivary glands, front taste (nucleus solitaries); exits through cerebropontine angle Geniculate- no synapse, sensory (taste, and external ear skin) Nervus intermedius- parasympathetic fibers to pterygopalatine ganglion (lacrimal gland and salivary gland); tast sensation from anterior tongue (chorda tympani) External ear conncets with trigeminal in brain stem Salivary glands Parasym, salivary, synapsel; combine with sensory to make intermedius Spinal nucleus- pain/temp Internal genu- facial axons loop around abducens nerve Internal auditory canal Great Petrosal lacrimal gland with maxillary Stapedius- vibration, hyperacousis if injured Chorda tympani- mandibular (v3) for salivary glands; also tongue taste Passes through stylomastoid foramen- facial muscles (lesion= palsy) Central Facial palsy- forehead fibers crossed and uncrossed, upper lesion still frown, lower cannot frown and droopy eyelid Both sides cross to bottom (left side lesion left bottom of face still moves), top gets from both sides ( lower left lesion will affect left bottom face and partial upper left face, still gets signal from right upper though) Crocodile tears syndrome- crying while eating; lesion by geniculate ganglion Complete destruction of facial nucleus paralyzes all ipsilateral face muscles (bells palsy- tumors, sarcoidosis, aids, lyme disease, herpes zoster; try to close eyelid and your eye goes up) mumps or stabbing of stylomastoid foramen flaccid paralysis; chorda tympani lesion- no taste Corneal reflex- sensory (ciliary nerves, nasociliary, ophthalmic, trigeminal) interneurons process; motor (facial nerve) Vestibulocochlear nerve

Hearing cochlear, balance vestibulo Nerves pass through acoustic meatus to brain stem in middle cerebellar peduncle Acoustic neuroma; vestibular schwannoma at cerebellopontine angle ( cant hear, tinnitus, disequilibrium; facial palsy, no tears; trigeminal cerebellar symptoms) Glossopharyngeal nerve- 3rd branchial; motor (ambigus nucleus); parasympathetic ( inferior salivatory nucleus, tympanic plexus petrosal nerve and otic ganglionparotid gland) Jugular foramen by vein Tympanic nerve- anastomosis with mandibular and parotid Posterior tongue; unipolar cells in inferior ganglia go to solitary tract (also receives from facial and vagus) and thalamus cortex Pharyngeal branchiomotor/sensory of pharynx Lingual- tongue senses Carotid sinus- viscerosensory chemoreception of blood pressure and gas Gag reflex- nerve IX for sensory and X does motor; if one piece is injured then no reflex; oropharynx stimulated; IX> solitaries> ambigus> and vagus; contract pharynx soft palate and fauces; can even trigger vomitting Vagus- motor from ambigus nucleus (soft palate and pharynx) visceral efferent (dorsal motor nucleus to terminal ganglia for heart rate to left colic flexure) Epiglottis sensation to solitary tract Auricular branch (sensory); pharyngeal (pharynx motor.sensory); superior laryngeal (motor/sensory) Inferior laryngeal Pharyngeal Lesion- uvula deviates to opposite side; soft palate rises when they say ah Laryngeal lesions- hoarseness Transection is fatal Cough reflex- irritation stimulate laryngeal and trigeminal sensory nuclei medullary respiratory/nucleus ambigus; coughing by contraction of intercostal and abdominal muscles (intercostal and phrenic nerves) against closed glottis (controlled by vagus) Sneezing- nasal mucosa stimulate opthalmi/maxillary trigeminal sharp inhalation and the exhalation agasint closed oropharyngeal isthmus by palatoglossus forcing air through nose Swallowing- oropharynx stimulates glossopharyngeal> solitaries and ambigus; coordinate palate pharync and larynx Soft palate closes nose off; larynx raised and narrowed with a closed epiglottis; pharyngeal plexus controls swallowing Accessory nerve- somatomotor sternoclastoid and traps; technically in spinal cord so not a true cranial nerve; exits between spinal roots and ascends to nucleus ambigus and join vagus Lesion- cant turn head to contralateral side; wing scapula Hypoglossal-somatomotor supply of internal/external tongue muscles; medulla and pops out between pyriamids and olives; Tongue deviates towards lesion

BRAIN STEM

Truncus cerebri made up of mesencephalon (midbrain) pons myelencephalon (medulla) Ascending descending tract/ nuclei; motor centers; reticular formation Pyramidal tract Corticospinal- motorcortex> tracts (lateral cross) Corticobulbar fibers- accompany fibers Eye movements not on pyramidal tract Medial lemniscus system- discriminative touch (light merkel) presseure (mesiner) vibration (pacini) 2nd neurons decussate up in medulla medial meniniscus 3rd vpl of thalamus internal capsul post central gyrus From vertical to horizontal as it ascends Spinothalmic- pain and temp; go to dorsal horn, decussate in white commissure; lateral columns ascend then go to vpl in thalamus internal capsule post central gyrus Where/how painful Collaterals to reticular formation and other parts of thalamus and limbic; creates emotions of pain Proprioception- muscles spindles golgi tendon organs, ruffini corpuscles, pacini; dorsal column in gracile and cuneate nuclei; vpl thalamus; gyrus (medial lemniscus system) Lateral column cpinocerebellar (ataxia) Head somatosensory- trigeminal nerve crosses (discriminatory pontine trigeminal; spinal trigeminal cross in pons) before thalamus Proprioception mesencephalic trigeminal (different ganglion) massester reflex Tectum- quadregeminal plate; posterior Tegmentum- anterior aqueduct; somatomot oculomotor nucleus Substantia nigraCrus cerebri- descending pathways; motor deficits in face, mouth body Periaqueductal pain modulation; fear reaction; opiate receptors Ipsilateral brainstem- cranial nerve nuclei exiting fibers Contra lateral- descending fibers; extremities Weber syndrome- ventral damage usually posterior cerebralartery infarction ; ipsilateral paralysis of extraocular muscles; dilation of pupil; contralateral extremity paralysis; weak lower face, tongue points to lesion Claude syndrome-central lesion; ipsilateral eye deficits (down and out); dilated pupil; contra lateral ataxia, tremor, incoordination (red nucleus damage) Benedict- weber plus claude Pons Medulla- autonomic respiration circulation, gi; decussation to pontine sulcus CN9-12; inferior cerebellar peduncle Includes fasiculus grcilis cuneatus and nucleus; medial leminiscus decussation; spnothalmic tracts Descendin- pyramidal decussation Blood supply PICA, ASA, PSA, VA, AICA Pica is most important; Lateral medullary Wallenberg- PICA insuffienciy; contralateral loss of pain and temp (anterolateral); ipsilateral pain and temp of face (spinal trigeminal tract) vertigo nystagmus (vestibnular nuclei); ipsilateral loss of taste (solitary nuclei) hoarseness and dysphagia (nucleus ambigus) horner syndrome

SpinalDorsal sensory; ventral motor Poliomyelitis- ventral horn paralysis Singles dorsal itching Rami-from nerve; region; mixed Roots pure form spinal cord Herniated disk- protrustion/prolapse of pulposus; lateral or medial Lumbar; can press on cauda equine (pain, muscle weakness of sciatic nerve; fecal urinary incontinence; sexual dysfunction; cant raise leg or flex knee; percussion L4 l5(weak dorsiflexion) s1 (ankle); minor strain ; Pain- overrides inhibition of fast fibers Gaba inhibit; Subtantia gelatinosa- raphe nuclei and locus coeruleus can inhibit pain in stress situation (PAG limbic system) Syringomyelia- enlarged spinal cnal; no more decussation (flaccid paralysis, weakness, atrophy, no reflexes) Anterolateral column- spinocerebellar tract; spinal ataxia Rubrospinal tract- feedback Vestibulospinal- balance Reticulospinal- inhibition of motor during sleep Brown sequard syndrome- ascending and descending fibers; everything below is ruined; ipsilateral posterior and corticospinal symptoms; spinothalmic contralateral symptoms; stab wound; no pain inhibition (contralateral hyperalgesia); paralysis

Degenerative disease Dementia- memory impairment, cognitive deficits, with consciousness; not normal aging; not dementia is dus to degeneration (infarcts give binswanger disease) Alzheimer- most common; insidious impairment of higher thinking, mood and behavior disorders; progressive disorientation, memory loss, aphasia; disability, mute, immobile; die from pneumonia or infection Mainly over 75 esp 85; rare before 50 (those tend to be heritable) Slight familial rfelationship I(mutations in enzymes) Accumulation of b amyloid from amyloid precursor protein (when its cut by bsite app cleaving; AB is created); accumulates forms amyloid fibril Down syndrome after 45 will get alzheimers because of app mutation Apolipoprotein e4 associated with risk and early onset; sorl1 late onset Ab aggregates alter neurotransmission; plaques neuronal death, inflammation altered communication Additionally hyperphosphorylation of tau microtubule; redistributes within neuron into dendrites and makes tangles fucking those neurons up Cortical atrophy, wide sulci, ventricular enlargement (hydrocephalus ex vacuo) plaques and tangles; start in entorhinalhippocampal isocortexneocortex Plaques- silver staining, central amyloid core, hippo, amygdala, neocortex; b amyloid Tangles- paired helices; remain after neurons die Frontotemporal dementia

Progressive deteroiation of language/personality; temporal /frontal lobes; memory distrurbance after (thats how you differentiate); inclusions separate varieties Parkinsons Diminished facial expression; stooped posture; slow voluntary movement; festinating gait (short quick step) rigidity, pill rolling tremor (many symptoms common to dopa disease such as dopa antagonists and toxin mptp) Parkinsonism- post encephalitic parkinsonism (flu)multiple system atrophy; progressive supranuclear palsy; corticobasal degeneration; Huntington Idiopathic parkinsons- have to exclude toxic or other etiology and show response to l-dopa Auto dominant (a synuclein)/recessive Lewy bodies with a synuclein Pale substantia nigra; loss of pigmented cells; lewy bodies in neuron (eosinophilic round with halo with a synuclein and ubiquitin) Ldopa- symptomatic; does not alter progression over time; becomes less effective causes its own motor function Dementia- 10-15%; mainly older; fluctuating, hallucinations; Huntington Inherited auto dominant; movement disorders, dementia, degeneration of striatum (caudate/putamen); kill in 15 years; motor before cognition; early forgetfulness; suicide and infections Jerky, hyperkinetic, chorea (involuntary); parkinsonism bradykinesia rigidity Mutation on 4p16.3 CAG repreat; more copies earlier onset (as early as teens); not disease related Spermatogenesis; paternal transmission with early onset; sporadic very rare Mutant protein stretches bind sequesters transcription factors reducing protein levels; mitochondria abnormalities (electron transport effects) neurodegeneration Aggregation causing apoptosis is possibility No one knows why neuro specific since this is found everywhere in body Small brain; caudate nucleus shrinks and mutamen; medial to lateral ; ventricles dilated; frontal atrophy; striatum levels correlate with severity Spinocerebellar degenerations- cerebellar/sensory ataxia, spasticity, sensorimotor peripheral neuropathy Degeneration of neurons; mild gliosis Many are caused by cag repeat (transcriptional regulation, aggregation, calcium homeostasis) Friedrich ataxia- auto recessive; children, gait ataxia, hand clumsiness, dysarthria (speaking); deep tendon absent; Babinski present; joint vibration loss; no pain/temp, light touch; pes cavus, kyphoscoliossis; cardiac, diabetes; whell chair bound; infections; GAA repeat Degeneration/gliosis of posterior column, neuronal loss, depletion of fibers Ataxia telangiectasia- Louis bar syndrome- cns, eye skin disease; AR inheritance; ATM gene; childhood ataxia; sexual delay; malignancies; high fetoprotein cea; low iga; telangiectasia; torpedoe cells (fat axons); cerebellar atrophy Motor Neurons Lmn-denervation atrophy, weakness, fasciculation Umn-paresis, hyperreflexia, spastic, Babinski

Amyotrophic lateral sclerosis lou Gehrig- most common; amyotrophy hyperreflexia; loss of both neuron types; lateral corticospinal tract degeneration; men slightly; middle age; some familial auto dominant; sod1 (superoxide dismutase) also gain of function by missense; there could be misfolding and apoptosis involved Anterior spinal, thin and gray (should be white); premotor gyrus atrophic, spare extraocular muscles Asymmetric hand weakness (dropping things, performing motor tasks) cramping spasticity; strength and bulk diminish; fasciculation; respiratory muscles and infections Bulbospinal atrophy (kennedy disease)- x linked adult onset; lmn; distal amyotrophy, dysphagia, fasiculations of tongue; androgen insensitivity gynecomastia, testicular atrophy, oligospermia; tri nucleotide mutation Spinal muscular atrophy- auto recessive; childhood; lmn; muscle fiber atrophy; most common is sma1 (werdnig Hoffman) at birth and kills as toddler Multiple systems atrophy- sporadic progressive adult onset; unknown cause; synuclein/ubiquitin glial inclusions Parkinsons- no lewy bodies Cerebellar- shrunken cerebellum; ataxia Progressive supranuclear palsy- hypokinetic, parkinsonism, abnormal eyes; hetergenous degeneration; 5-6/100,000; 50-70 yrs old; rapid progression; mainly spont but some familial (tau relations); basal gang, midbrain and pons accumulation of tau Wilson- no extraction of copper; lenticular nucleus; ar inheritance; brown putamen, neuronal loss; alzheim astrocytes; opalski

Myelin diseases Demyelinating vs dysmyelination Multiple sclerosis-autoimmune demyelinate; episodes of neurologic deficits; most common in us and Europe; any age but usually adulthood; usually women; frequency tends to decrease with some deterioration Environmental (ebv, herpes 6, vit d, sun)/gentic factors; 15x risk in families (HLADR2) Inflammatory plaques; tcell mediated delayed hypersentivity rxn; some axonal injury and neuronal death Myelinated fiber tracts, circumscribed, depressed, glassy gray tan ireegular lesions; firm centered on blood vessel; by ventricles, optic nerves, brain stem, cerebellum; active ongoing breakdown, astrocytes with debris, sparing axons, inflammation, complement, edema and cytokines; quiescent leave astrocytes and gliosis; shadow plaques remyelination, periphery, fails; blue cerebellum with chunks uncolored Episodes of new sypmtoms then remission; stepwise deterioration; unilateral visual impairment for a few days (first event rarely get full MS); brain stem shows CN involvement, ataxia, conjugate eye; spinal cord motor and sensory, bladder; decrease rate and severity not regain function for treatment

Csf has high g globulin (oligoclonal bands with ab against many targets), pleiocytosis, high protein; Methylprednisolone, intefreon beta, natalizumab, cyclophosphamide, methotrexate, azathioprin Acute ms Marburg- monophasic, fulminant rapid, children and young; massive rxn Tumefactive ms, presenting as neoplasm- single mass hemispheric; myelin loss; macrophages, astrocytosis, perivascular Balos- rare; children/young adults; waves of demyelination with myelination Schilder type- childhood; giant plaques Neuromyelitis optica (devics)- optic neuritis, acute transverse myelitis; time between symptom; necrosis, marked demyelination vertebral segments; csf with ig Acquired demyelination- monophasic with abrupt onset Acute disseminated encephalomyelitis- week or two after infection (mumps, measles, rubella, varicella, ebv, mycoplasma pneumoni, c jejuni, strep a, rabies shot), diffuse involvement (headache coma, ) rapid, 20% fatal; white matter affected Acute necrotizing hemorrhagic encephalomyelitis- worse, young adults, children; monophasic, viral immune disease; punctuate hemorrhages, fibrinoid necrosis in blood vessels Subacute sclerosing pan encephalitis- infection in oligodendrocytes by fucked measeles; variable latency; loose higher brain (now youre fucked); perivascular lymphoid; intranuclear inclusion measles; virus identification by pcr; die in 2 years Central pontine myelinolysis- nonimmune, in pons; rapid correction of hyponatremia; alcoholism electrolyte, osmolar imbalance; quadriplegia Toxic leukoencephalopathy- medications or drugs; cyuclosporine, methotrexate, bcnu, cytosine, fludarabine, cisplatin, ethanol, cocaine, ecstasy heroin; demyelination, inflammation, necrosis, mineralization Progressive multifocal leukoencephalopathy- JC virus in immunocompromised; papovavirus; AIDS Leukodystrophies- inherited dysmelinating disease; abnormal production or turnover; lysosomal peroxisomal enzymes, mutations; most AR inherit or x linked White matter becomes grey and clear; shrinks; can be patchy or occipital; but consumes everything, ventricles enlarge, grey matter changes; macrophages full of lipid Children born normal but miss milestones

Peripheral vestibular disorders Benign positional vertigo- particular head position, peripheral vestibular lesions; most common peripheral vertigo; head trauma; canalolithiasis (semicircular canal debris); brief severe vertigo; laying down on ear; resolves spontaneously; no hearing loss can be recurrent Nylen barany/ dixhallpike patient sitting with legs extended, rotate head; lie down quickly with head roatated, latent then nystagmus toward affected ear; up and down nystagmus is central system caused( semicircular canals); sit again and things are reversed Rotate head to move debris; vestibulosuppressant drugs Meniere disease- repeated vertigo, for minutes to days; tinnitus (ringing) and sensoneural hearing loss; sporadic rarely familial with anticipation (cochlin gene) adults, usually men; possibly due to endolyph hydrops; symptoms before acute vertigo attack (vertigo nausea, vomiting, recurring)stepwise hearing deterioration usually bilateral (worse hearing better vertigo) Nystagmus during attack; caloric testing shows abnormal restuls; hearing defecits vary; audiometry low frequency pure tone hearing loss, impaired speech discrimination and increase sensitivity to loud noises

Hydrochlorathiazide, triamterene; endolymphatic shunting, labyrinthectomy, vestibular nerve section Acute peripheral vestibulopathy- spont vertigo; inapparent causes; spont resolution; no hearing loss or CNS dysfunction; acute labyrinthitis/vestibular neuronitis possible; sometimes fever preceded; vertigo nausea, vomiting up to 2 weeks; some vestibular dysfunction is permanent; dont want to move head just lay down; nystagmus away from affected side; caloric testing abnormal; prednisone

Weber test- tuning fork; sensoneural (cochlea, or nerve) sound perceived at normal ear; conductive (external/middle ear) sound is localized to abnormal ear Rinne test- placing tuning fork next to ear and over mastoid and comparing (air should be louder) Cholesteatoma- expanding lesion of temporal bone; jeratin; proteolysis (looks like a huge clunmp of wax) Otis media- most common conduction in children; strep, External otitis- outer ear canal- swimmers ear pseudomonas, staph, aspergillus

Optic neuritis Inflammation of nerve; can be idiopathic; demyelination or inflammation of meninges; viral infection; unilateral happens within days (headache, tenderness eye pain especially when movement); central scotoma or blurry vision; fundus normal if inflammation behind disk; can see pupillary defect in affected eye; visual acuity will improve (methylprednisone) can be first sign of MS; toxins (alcohol, methanol, neuro syphyliis, b12 deficient) Arcus senilis- elderly; grey ring around cornea, cholesterol deposits Opthalmia neonatorum- conjunctivitis in newborn; neiserria gonn, chlaymidia Bacterial conjunctivitis- pain,pus, no blurriness; staph, strep, haemophilius Viral conjunctivitis- watery; adenovirus (pinkeye)hsv 1 dendritic ulcers Allergic conjunctivitis- seasonal itching Acanthamoeba- keratoconjuctivitis- contacts not cleaned Stye- eyelid infection, staph Chalazion- granulomatous, often disappear Orbital cellulitis- periorbital red and swollen; sinusitis; staph fever; Glaucoma Open angle- decreased outflow; bilateral aching, pathologic cupping of optic disks; night blindness, loss of peripheral giving tunel visions (beta blockers) Closed angle- narrowing of chamber angle; mydriatic agent (dilation); uveitis, lens dislocation ,sever pain with light, blurry visision, red eye; fixed unreactive pupil Tabes dorsalis- neurosyphilis; sensory symptoms; posterior roots and degeneration of columns; unsteadiness, somatic pain, urinaryincontinence; visceral abdominal pain; no vibration or joint position in legs; ataxic gait Romberg sign; no deep pain; flaccid enlarged bladder; tendon reflexes lost; hypotonic limb; hypertrophy (charcot) jointsargyll Robertson pupils, optic atrophy, opthaloplegia; 4-7 years into disease Can also present with general paresis (chronic meningoencephalitis; active infection, dememtia, psychiatric disorders, memory loss, psychosis, seizures, strokes

Syringomyelia- cavitation; location determines stymptoms; sensory loss at lesion including pain and temperature; light touch good; can have ulcers, scars, hyperhidrosis; weakness and wasting dur to anterior horn involvement; loss of tendon reflex; cape like loss of senses; t1 segment can give you horner; lower brainstem damage = tongue wasting, vocal cord paralysis Communicating- central canal and cavity communicate; hydro dynamic disorder; developmental anomalies of roamen magnum (foramen chiari); chronic arachnoiditis; surgery Noncommunicatin- cystic dilation of cord, not communicating with csf; trauma, tumors; can be interval of years Burn your hands without notiticing; no sensory loss in als Subacute combined degeneration- impaired absorption of b12; pernicious anemia, GI surgery; sprue; fish tapeworm; vegan diet; distal paresthesias, weakness; spastic paraparesis and ataxia; lhermittes (bend head forward get tingles); macrocytic megaloblastic anemia Nerve root lesions Lumbar disk prolapse- pain in back and radiculopathy in leg (numbness and paresthesias), motor deficit (l5= dorsiflexion; s1= plantar) cant move spine, local tenderness, spasms; cant raise legs while supine (lesegue hamstring spasm) sphincter involvement needs surgery Cervical disk prolapse- doesnt need trauma, pain in neck and arm; worse with head movement; lateral herniation sees motor/sensory deficits; spinal cord involvement paraparesis, impaired sphingter, need CT, mri Cervical spondylosis- pain stiffness in neck and arms; may have deficit usually in legs; cervical disk degeneration andherniation; calcification; head restriction; c5/6 so weakness of shoulder arm region, pain and sensory loss and possibly no tone; osteophyte formation; narrow disk spaces Traumatic avulsion of nerve roots Erb ducheene paralysis- c5/6 avulsion at birth; traction on head during delivery or injury; no should abduction or elbow flexion; internal rotation and forearm pronation; no biceps jerk Klumpke paralysis- c8/t1 paralysis of hand and fingers; horners syndrome; fall and tried to catch yourself Neuralgic amyotrophy- shoulder pain then weak numb arm; c5/6; muscle wasting; vaccination, injury, infection Cervical rib syndrome- c8/t1 roots; compressed by cervical rib from c7; affects hand muscles especially thumb; subclavian artery may be compressed (adsons test- radial pulse weakens when seated patient turns to affected side and inhales) supraclavicular bruit Radicular pain Localized to a nerve root; coughing sneezing make worse; pressure and stretching root increases pain; raising legs, flexing neck; paresthesias and numbeness Thalmic pain- contralateral half of the body; burning; emotional stress; while recovering from sensory deficit; mild stimulation elicits a lot of pain (dejerine roussy syndrome) Back /neck pain- can be local or referred; posture changes, spasms Low back pain Trauma- exertion/activity; no bracing; improves with rest; spasms of lumbar muscles; heat, bed rest; nsaids, diazepam; Lumbar osteoarthropathy- late in life; activity; surgical corset; Facet joint disease Entrapments

Median nerve in carpal tunnel-preggos, arthritis, trauma; pain and tingling; weakness cant sleep; tinel sign; phalens Radial nerve- crutches; alcoholics sleeping on floor Peroneal hit on top of knee; recovers Tarsal tunnel- burning in the foot at night Femoral neuropathy- diabetes, vascular, bleeding; weakness of quads; no knee reflex