Nose and Mouth 

Chemical Senses

• gustatory (taste): detects ingested molecules-tastants; primarily water and fat soluble molecutes (quantity, quality and safety)
• Olfactory (smell): detects airborne molecules-oderants; info about self and other people; odorants involve social interaction, reproduction, defensive behavior, feeding behavior
• trigeminal (chemosensory irritant): noxious chemicals that come into contact with mucus and skin in nose and mouth

Taste Buds/Papillae

• taste buds found in papillae
• 3 types of papillae: fungiform (ant 1/3 of tounge), foliate (along side of tongue), and circumvallate (9 at the back)
• 4000 taste buds on surface of tongue, pharynxm larynx, and upper esophagus
• CN VII(tympani) get info from fungiform in front
• CN IX and part of VII get info from foliate
• CN X (laryngeal) get info from circumvallate, epiglottis and esophagus
• 250 circumvalate taste buds, foliate 600 taste buds, fungiform 3 taste buds

Taste Buds

• taste cells, supporting cells and basal cells
• taste cells are epithelial cells (not neurons)
• replaced every 10-14 days from basal cells
• receptors are located on microvili on each taste receptor cell
• microvili extend into taste pore, bathed in saliva
• each receptor cell only responds to 1 type of tastant
• serotonin is one of the NT that activate the gustatory afferent axons

Taste Transduction

• taste cells are polarized epithelial cells - no axon and dendrite (apical and basal domains)
• apical end receptors activation ion channels or GPCR (only located thered)
• Graded receptor potentials from Apical to Basal
• this depolarization: Voltage gated NA channels, ect, to release serotonin at basal end
• also have TRPM channels somewhere

Tastants

• non volatile, hydrophilic molecules soluble in saliva
• perceived intesity of taste proportional to conc
• threshold conc for ingested tastants is high for conc of salts and carbohydrates to allow for adequate intake 
• noxious subs(quinine, bitter plant) have very low thresholds
• 5 main tastes: sweet, salty, sour, bitter, unami(msg)
• chemical mixtures produce new tasts(astringent, pungent, metalic) and overriding of protective responses to aversive tasts 

Taste Receptors

• Salt: ion channel, amiloride-sensitive Na channel
• Acids(sour): H sensitive TRP channel, ion channel
• sweet: uses T1R2 and T1R3 GPCR
• amino acids(unami): T1R1 and T1R3 GPCR (Gq) that activates TRPM5 Ca ion channel
• bitter: T2R GPCR(Gq) receptor that uses gustducin that activates TRPM5 Ca ion channel

Primary Taste Afferents

• CN X (Vagus): pharynx-nodose ganglion
• CN IX (Glossopharyngeal): lateral posterior tongue - petrosal
• CN VII (Facial): anterior tongue - geniculate ganglion
• projections run through solitary tract in medulla (rostral and caudal region) (three tongue afferents end at rostral)
• caudal region recieves branches of sub-diaphragmatic branches of vagus(gastric motility)
• posterior region of n solitarius gets visceral sens info (integration of taste and visceral sens, gustatory-visceral reflex arc)
• taste pathway is ipsilateral

Cerebrum Pathways

(taste)

• ipsilateral pathway from tongue
• from the solitary tract it goes up the central tegmental tract to VPM (solitary ends at medulla/pons)
• ventral posterior medial (VPM) nucleus of thalamus
• next to insular cortex on same side and also pathways to the frontal cortex (frontal operculum) 
• secondary cortical taste are: obitofrontal cortex: combines visual, somatic sensory, olfactory, and gustatory for satiety
• insualr and frontal cortex can go to hypothalamus and amygdala to control feelings

Olfactory Epithelium

• receptor cells with axons going up into the olfactory bulb
• microvili(cilia) are in mucus membrane on the apical end of the receptor cell (contain the receptors to oderants 
• dividing stem cells that give rise to new receptor cells
• bowmans gland that produces mucus and other supporting cells
• each receptor cell basically codes for one specific odor with little overlap

Olfactory Transduction

• uses G proteins entirely (only sensory system that uses only GPRC): 
• slow system
• Use Gs that then go on to activate ion channels through A/C for depolarization

Olfactory bulb

• olfactory nerve prjects ipsilaterally to olfactory bulb on ventral aspect of cerebral hemisphere
• olfactory nerve terminate in the glomerulus of bulb
• mitral cell and tufted cell carries info from glomerulus to lateral olfactory tract 
• each glomerulus is specific for certain odors
• periglomerular cells inhibit one glomerulus and allow the other to activate (lateral inhibition)

Central Olfactory 

• no thalamic relay from primar receptor to neocortex
• olf ino sent to thalamus in route to association areas of neocortex
• olfactory bulb sends info to pyriform cortex, olfactory tubercle, amygdala, and entorhinal cortex
• these then effect orbitofrontal cortex, thalamus, hypothalamus and hippocampal formation
• piriform cortex + association areas of neocortex(orbitofrontal cortex) needed to associate odors with other sensory stimuli 
• olfactory memory is in entorhinal cortex

olfactory tubercle

• involved in multisensory 
• reward behavior
• recieves input from olfactory bulb and sends it out to other areas 

Clinical notes: smell

• anosmia: total loss of sense of smell
• hyposmia: reduced sense of smell
• olfactory hallucinations: epileptic seizure involving anterior medial temporal lobe (pyriform and entorhinal cortices

Skeletal Muscle Contraction

Lower Motor Neurons

• initiated by lower motor neurons in spinal cord and brainstem
• cell bodies of LMN located in ventral horn of spinal cord and in motor nuclei of the cranial nerves in brainstem
• LMNs also called alpha motor neurons
• alpha motor neurons send axons directly to skeletal muscle through ventral roots of spinal cord, spinal peripheral nerves and via cranial nerves

Somatotopic arrangement of

local circuit neurons

• in spinal cord gray matter
• postural muscles: medial local circuit neurons- medial lmns in ventral horn(bilateral conectivity)
• fine extremeties: lateral region of intermediate zone (ipsilateral local connections)-independent control of local extremities
• fine extremity doesnt cross, doesnt have to move fingers of both hands at same time

Two typs of motor neurons

• gama motor neurons: innervate muscle spindles, sensory receptors; intrafusal fibers
• alpha motor neurons: innervate extrafusal muslce fibers

Motor unit and size principal

• motor neurons with small cell bodies: few muscle fibers
• motor neurons with large cell bodies: large number of muscle fibers
• as the strength of synaptic stimulation increases, recruit more motor units(starting at the samller ones towards the larger ones) 

Types of muscle contraction

• isotonic contraction: muscle shortens during contraction, depends on the load and the inertia of the load
• isometric contraction: muscle does not shorten during contraction; changes only in the force of muscle contraction

Reflex definition

• specific, stereotyped, motor response that occurs as a result of specific sensory input
• involuntary, but many can be modulated by higher centers and other inputs
• at minimum, consists of sensory neuron, motor neuron adn a single synapse btw the two (monosynaptic)
• reflexes maintain a nearly automatic reaction to certain sensory stimuli

Myotatic Reflex

(stretch Reflex)

• stretch or lengthening of the muscle spindle results in contraction that shortens that muscle
• in patellar reflex, stretching muscle activates spindle that transports info to spinal cord
• spindle synapses on both interneuron and a alpha motor neuron to the extensors, activating them
• the intereuron then inhibts the alpha motor neuron that go to the flexor muslces, causes relaxation of them
• this involved both monosynaptic and disynaptic connections

muscle spindle

• Grpup I and II afferents
• convey info about the length of the intrafusal muscle fibers and rate of change of length
• this conveys information about length and change in length of extrafusal muscle fibers
• gamma motor neurons (efferent) regulate contraction of the intrafusal fibers
• spindle afferents cannot provide info about changes in muscle length w/o gama fibers (gamma motor neurons readjust sensitivity/response of muslce spindle afferents)

Inverse Myotatic Reflex

• increased muscle tension activates Golgi tendon organ
• this uses Ib afferents and Ib inhibitory interneurons
• this activates inhibitory interneurons in spinal cord, which inhibits further contraction and excites the antagonistic muscles
• this is called autogenic inhibition
• regulates contractile force

Withdrawal (flexor) and crossed-extensor

reflexes

• stimulation of cutaneous receptor
• an afferent fiber from nociceptor A delta carries info to the spinal cord and attaches to four interneurons, with two crosses the spinal cord to the other side
• this then causes a flex of the leg that the stimulus came from and an extension (to support body weight) on the other leg 

Lower Motor Neuron Syndrome

• symptoms resulting from damage to LMNs in brainstem and spinal cord
• damage to LMN cell bodies or their peripheral axons: paralysis (loss of mvnt); paresis (weakening of muscles)
• loss of reflexes(areflexia)-results from interruption in efferent motor limb of reflex arc
• loss of muscle tone: depends on monosynaptic reflex arc which links sensory input (spindle) to LMNs
• later effects: muscle atrophy due to disuse, spontaneous twitches due to de-innervation of muscle or abnormal excitability of damaged motor neuron axons

Upper Motor Neuron Locations

• motor cortex (in frontal lobe): voluntary and skilled movements
• brainstem: posture and body position, locomotion, orientation to sensory stimuli, emotional expression
• targets are alpha motor neurons, gama motor neurons, and interneurons
• most descending control first go to local circuit neurons, not lower motor neurons 

Laterality of Upper motor neurons

• lateral system is crossed
• medial system is bilateral the axons can recross, have to be more cooridnated btw the two sides unlike the lateral system

Primary Motor Cortex (M1)

• brodmann's area 4, in precentral gyrus
• UMN projections: the corticospinal and corticobulbar projections arise from layer 5 of cerebral cortex
• neaur absence of corticolayer 4
• Betz cells found in layer five and connect to lower motor neurons directly, responsible for finest motor movements

Motor Cortex

• voluntary movements
• primary motor cortex: precentral gyrus and paracentral lobule; execution of fine skilled movements
• premotor cortex: frontal lobe, anterior to primary motor cortex; planning and selecting movements 

corticospinal tract

(pathway)

• origin: cerebral cortex
• termination: spinal cord ventral horn
• axons traverse: corona radiata
• internal capsule, posterior limb
• cerebral peduncle (crus cerebri, basis peduneuli)
• fiber bundles in base of pons
• pyramid: to pyramidal decussation and lateral corticospinal tract or coninuing uncrossed in ventral corticospinal tract

Corticobulbar tract

(pathway)

• origin: cerebral cortex
• termination: brainstem motor nuclei
• axons traverse: corona radiata
• internal capsule, posterior limb
• cerebral peduncle(crus cerebri, basis pedunculi)
• fiber bundles in base of pons
• pyramid
• travel with corticospinal fibers until they are close to level of target, then split off and travel across brainstem to target area
• corticorubral(to red nuc) and corticopontine(to pontine nuc) also traval with corticobulbar (these are not UMN though)

Corticobulbar tract

Targets

• motor V nuclei
• facial nuclei
• nu. ambiguus
• hypoglossal nuclei
• corticobulbar system is bilateral, so projections to both sides from one nuc

Control of Facial Muscles

Corticobulbar tract clinical issues

• left side of face: upper and lower parts recieve seperate innervation via CN VII
• lesion of CN VII yield sparalysis weakness of whole side of face 
• lesion of corticobulbar path yields paralysis limited to lower face (upper face still innervated by intact corticobulbar tract from other side, bilateral)

Premotor Cortex

• brodmann's area 6
• as wella s specialized contributions from 8, 44, 45, 23, 24

Lateral Premotor Cortex

• for movements based on external events
• lesions: may lose ability to follow verbal commands or sensory cues

Medial Premotor cortex

(supplementary motor cortex)

• for movements based on internal events
• spontaneous movements and movements from memeory
• lesions: reduction in self-generated movements

Upper motor neurons

(brainstem)

• in vestibular nuclei and reticular formation for balance and posture
• in superior colliculus for gaze control

Medial vestibulospinal Tract

• originates from medial vestibular nucleus
• driven by semicircular canals
• terminates medially in ventral horn of cervical sp cord
• reflex action on neck mesucles to control head position

Lateral Vestibulospinal Tract

• originates from lateral vestibular nucleus
• driven by otolith organs
• terminates medially in ventral horn of sp cord
• reflex action on trunk and proximal limb muscles, especially extensors

Reticular Formation

• spread throughout the core (tegmentum) of brainstem
• includes nuclei associated with autonomic system(cardio), coordination of reflexes mediated by brainstem cranial nerves, modulation of pain pathways, chemical pathways, regulation of sleep, wakefullness and arousal, and motor control(eye and reticulospinal)
• lower areas-in caudal pons and medulla-include the origins of the reticulospinal tracts

Parts of the Reticular Formation

• mesencephalic and rostral pontine: modulates forebrain activity
• caudal pontine and medullary reticular formation: premotor coordination of lower somatic and visceral motor neuronal pools

Pyramidal and extrapyramidal

• pyramidal named because axons travel in the pyramids(essentially corticospinal and corticobulbar tracts)
• extrapyramidal: other descedning pathways plus the basal ganglia and their connections

Origins of pyramidal tract

• 1/3 from M1 (primary motor cortex)
• 1/3 from premotor areas (premotor and supplementary motor cortex)
• 1/3 from primary somatosensory cortex 
• ^makes it not entirely motor

UMN syndrome

• weakness (paresis) or paralysis
• spasticity: hypertonia and hyperreflexia (increased muscle tone and stretch reflexes)
• UMN lesion causes spastic paralysis 
• contrast with flaccid paralysis (LMN lesion)
• paralysis is people cannot make voluntary muscle movnts

decerebrate and decorticate

rigidity

• actually type of spasticity
• decerebrate is upper pontine damage and has arms exted at side with wrist and fingers flexed
• decorticate is upper midbrane and has arms flexed towards check at elbow, and wrists and hands flexed

Signs of upper motor neuron(UMN) syndrome

• weakness or paralysis or
•  spasticity: hypertonia and hyperflexia
• perhaps babinskis sign, clonus, loss of fine voluntary movements, reduced superficial relfexes

Apraxia

• loss of coordination and ability to perform complex series of movements
• caused by lesion in just premotor cortex
• pre-motor cortex is frontal lobe, anterior to primary motor cortex and involves planning and selecting movements

Spinal Shock

• UMN syndrome masquerading as LMN
• after a sudden injury of UMNs, particularly with a lesion in cortex or internal capsule, the initial clinical picture is different: flaccid muslces, hypotonia and hyporeflexia
• all deficits contralateral to the lesion
• over time=days to weeks- the picture changes to classic UMN syndrome

Alternating hemiplegia

• hemiplegia: paralysis on one side
• alternating: different sides at different levels
• seen with brainstem lesions: can involve III, VI, VII, XII

Dorsal Basal ganglia

• consists of caudate nu, putamen, and globus pallidus
• striatum is caudate nu and putamen
• lenticular nucleus is putamen and globus pallidus

basal ganglia circuitry

(inputs)

• most enter the striatum (caudate + putamen)
• most from cerebral cortex
• some from intralaminar nu of thalamus
• these inputs are excitatory 

basal ganglia circuitry

(outputs)

• most originate from GPi (globus pallidus, internal)
• some from SNr (substantia nigra, pars reticulata)
• major targets are VA (ventral anterior nu) and VL (ventral lateral nu) of the thalamus
• additional output to superior colliculus and reticular formation
• these outputs are inhibitory and use GABA (this means that Basal ganglia inhibit movement)

Disinhibitory circuit

• found in basal ganglia
• under normal conditions the globus pallidus(i) has an inhibitory (GABAergic) effect on VA/VL of the thalamus 
• the striatum has an inhibitory (GABAergic) effect on the globus pallidus, which would stop GP(i) inhibitory effects
• disinhibitory circle is the direct pathway (inhibits BG output, so increases movement) (indirect pathway uses subthalamic nuc and does the oposite, inhibits movnt)

Basal Ganglia Circuitry

• The BG circuits are uncrossed. Right BG affects the right motor cortex
•  Because right cortex controls left body, right BG affect movements on the left side of the body
• BG circuits use mutiple NT: glutamate, GABA, ACh(in striatal interneurons, dopamine (in SNc neurons that project to striatum)
• BG disorders either cause hypokinetic(lack of movt) or hyperkinetic(involuntary movts), not paralysis

Hyperkinetic Disorders

• characterized hy dyskinesia (unintentional movements)
• 3 main types: ballism (large-amplitude, violent movements of an entire limb), chorea(jerky, dancelike movements), athetosis (worm like writhing movements)
• choreoathetosis is a common term indicating combined traits

Hemiballism

• hyperkinetic disorders
• ballism restricted to one side of the body
• results from lesion of the subthalamic nucleus
• damages indirect pathway. the indirect pathway normally reduces movements; so damaging it leads to spontaneous movements
• right basal ganglia, right motor cortex, left side of the body

Huntingtons Disease (HD)

• hyperkinetic disorder
• loss of striatal neurons 
• major motor symptom is chorea
• progressive dementia
• autosomal dominant inheritance
• gene has been identified, but no treatment yet 

Parkinson's Disease (PD)

• hypokinetic disorders 
• akinesia
• bradykinesia
• rigidity
• resting tremor (contrast with intention tremor)
• loss of dopamine (DA) neurons in the substantia nigra, pars compacta(loss of nigrostriatal pathway)

Nigra-striatum pathway

• uses dopamine from the substantia nigra pars compacta
• this excites the striatum, activating the direct pathway (D1 receptors) and inhibiting the indirect pathway (D2 receptors)
• direct pathway is less active in parkinsons because loss of Dopamine in SNpc
• indirect pathway is more active in parkinsons

MPTP

• drug administered in monkeys
• causes loss of nigrostriatal neurons and appearance of Parkinsons disease
• was found in heroin in the 90s, causing parkinsons in young people 

Treatment of Parkinsons

• replace dopamine with drugs
• transplant DA producing cells into lateral ventricles that pour DA into caudate nuc
• surgically lesion GPi or subthalamic nu
• deep brain stimulation

Cerebellum

(a comparator)

• affects all movements, required for smooth, coordinated movnts and motor learning
• works by comparing:
• inteded movment(info from cortex)
• to actualy movement(sensory system inputs)
• and sending corrective signals to Upper motor neurons

Deep Cerebellar Nuclei

• from medial to lateral: fastigial, globose, emboliform, dentate (big squiggle that you can see gross)
• globose and emboliform are combined called the interposed nucleus

Cerebellar Peduncles

• SCP: brachium conjunctivum: mostly output
• MCP: brachium pontis: input (from pontine nuclei)
• ICP: input and output
• restiform body (bulk of ICP): spinal cord, inferior olivary nuc, and reticular formation
• juxtarestiform body (ICP): connections of cerebellum with vestibular system

Cerebellum Inputs

• climbing fibers: from inferior olive; axons leave inf olive, decussate, enter via ICP
• mossy fibers: all other inputs; spinal pathways, vestibular nerve and nuclei, pontine nuclei
• each fiber sends one branch to a deep cerebellar nucleus and one branch to the cerebellar cortex

Cerebellum outputs

• originate from the deep cerebellar nuclei
• axons project out of cerebellum through superior and inferior cerebellar peduncles
• targets include: ventral lateral (VL) of thalamus, reticular formation, red nucleus, vestibular nuclei, superior colliculus
• **there is a small portion of cerebellar output that originates from cells in the cerebellar cortex***

Cell types of the cerebellar cortex

• inhibitory cells: purkinje, basket, golgi, and stellate
• excitatory cells: granule
• three layers, molecular layer(superficial), purkinje cell layer, and granule cell layer

Inhibitory cortical loop

(cerebellum)

• climbing fiber contacts purkinje cell
• mossy fiber ends in glomerulus(contacts granule cell)
• granule cell excites purkinje and others
• purkinje cell inhibits deep nuclei
• (depends on balance of excitatory fibers and input from cerebellar cortex)

Major Sings of Cerebellar Lesion

• ataxia-lack of coordination: delays, errors in range(dysmetria), errors in rate or rhythm
• intention tremor (during intentional movement)
• additional clinical signs: hypotonia, dysmetria, dysarthria, dysdiadoehokinesia,decomp of movnt, lack of cheek, and nystagmus

Functional Subdivisions of Cerebellum

• vestibulocerebellum: input from vestibular system (the focculonodular lobe)
• spinocerebellum: input from spinal cord (vernis area)
• cerebrocerebellum: input from cerebral cortex via pontine nuclei (lateral hemispheres)

Localization of cerebellar disease

• vestibulocerebellum: flocculonodular lobe: problems with balance and eye movments, nystagmus may be present
• spinocerebellum: vernis/fastigial nu: body sway, dysarthria
• spinocerebelllum: paravernis interposed nu: limb ataxia, intention tremor
• cerebrocerebellum: lateral hemisphere/dentate: delayed initiation; decomposition of movnts
• chronic alcohol use causes degeneration of vernis in anterior lobe

Parkinsons Disease

Epidemiology

• incidence 1/1000
• usually sporadic (may be familial influence)
• onset usuallly > 50 years of age
• males > females
• progressive from onset (variable rate and results)
• 3 signs are bradykinesia, tremor, and rigidity
• lewy bodies, decrease in substantia nigra

Chorea

• greek for to dance
• involuntary, arrhythmic movements of a forcible, rapid, jerky type
• simple or elaborate
• purposeless but may be incorporated into deliberate movements
• anatomic basis unkown(caudate and putamen in huntingtons)

Athetosis

• varient of chorea (hyperkinetic)
• greek for unfixed, changeable
• slow, sinuous, purposeless movments
• flow from onte to another

Ballism

(Hemiballism)

• variant of chorea
• chorea limited to one side with violent, flinging movements
• lesion in contralateral subthalamic nucleus

Huntington's disease signs

• chorea: face, arms, legs and/or trunk
• dementia: gradual loss of thought processing and acquired intellectual abilities(memory, abstract thinking, judgement)
• emotional: agitation, personality changes
• caused by mutation of gene IT15 on chromosome 4(huntin protein)(CAG repeats)
• destroys caudate and putamen

Dystonia

• neurologic syndrome wint involuntary sustained muscle contractions causing abnormal postures and twisting and repetitive moment
• etiology unkown: possibly degenerative and gentic, probably polyfactoral
• focal dystonia (eyelids, neck, writers cramp)

Tics

• sterotypic repetitive non rhythmic jerklike movment(may be simple, complex or vocal)
• usually preceded by a sensory urge to move affected body part
• can be supresssed voluntarily but may build to a cresendo and result in flurry of involuntary tics
• may be secondary to identificable etiology(infections, drugs, toins) or primary(gilles de la tourettes syndrome)
• gesturing obscenely(cpropraxia) is a complex tic

Tourette's syndrome

• most common tic disorder-up to 3% of school age children
• diagnostic criteria: multiple motor tics, one or more vocal tics, tic present ofr at least one year, onset less than 21 eyars of age, no other identifiable causes
• usually associated with behavior abnormalities(OCD or ADD)
• possibly involves genetic and dopaminergic system in basal ganglia

Tremor

• most common movement disorder
• rhythmic involuntary oscillatory movement of a body part
• may be sole manifestation of a single clinical entitiy
• may be part of a larger spectrum of symptoms of a disease (Parkinsons)
• rest tremor and action (postural or kinetic) tremor 
• simple kinetic tremor durally all range of movement and intention is increased closer to goal of movement(cerebellar disease)

Essential Tremor

• most common type of tremor: 2% of population over 60
• autosomal dominant
• psotural or simple kinetic tremor
• slowly progressive
• involves hands, fingers, wrist, forearm, head, voice, tongue, chin, rarely legs
• worse with stress, emotion, and fatigue
• better with alcohol

Types of eye movement

• saccades: to acquire a target, voluntar or involuntary (reflex)
• smooth pursuit- to "track" a target 
• vergence-for foveating at different distances
• vestibulo-ocular: compensate for head movnts, good for short and/or fast movnts
• optokinetic: reflex nystagmus occurs as a large part of the visual scene moves slowly. cycle of tracking(smooth pursuit) and acquiring new target (saccade)
• fixation: actually an active process 

Rotational movements

• intorsion (top of eye toward the nose)
• extorsion (top of eye away from the nose)
• inferior oblique extorts when eye is abducted and elevates when eye is adducted
• superior rectus intorts when ee is adducted
• inferior rectus extorts when eye is adducted
• superior oblique intorts when eye is abducted and depresses when eye is adducted 

Gaze Centers

• Horizontal gaze center: paramedian pontine reticular formation (PPRF) in the pons; near abducens nucleus
• right PPRF does right eye movements and left left
• vertical gaze center: rostral interstitial nu of the medial longitudinal fasciculus(riMLF) in the midbrain

Paramedian Pontine Reticular Formation

(PPRF)

• activate Right PPRF
• this activates right abducens (CN VI) nucleus
• activate R lateral rectus
• inhibit R III via inhib internuclear neuron (medial rectus)
• at same time internuclear proj to left III to activate the left medial rectus
• Right eye abducts and left eye adducts
• MLF lesion effects both eyses; some nystagmus on L gaze (happens in Multiple slcerosis)

Vertical Eye movements

• vertical gaze center (riMLF)
• internuclear connections via MLF
• complex cominations of muscle activation

Control Centers for saccades

• superior colliculus (reflex saccade)
• frontal eye field (FEF): in brodmanns area 8, a region of the frontal lobe just rostral to premotor cortex (voluntary saccade)
• supplemental eye field: anterior end of supplemental motor area
• parietal eye field: in parietal lobe; especially important for visual attention

Smooth pursuit

• a voluntary reflex
• visual sensory pathway and visual cortex
• the where stream of visual info
• frontal and parietal eye fields
• superior colliculus
• gaze centers
• cerebellum
• possibly vestibular
• needs moving target 
• if damaged cant follow it smoothly, must make a series of saccades

Prevertebral Ganglia 

• unpaired, in front of spinal cord
• aorticorenal ganglion
• celiac ganglion
• superior mesenteric ganglion and inferior mesenteric ganglion
• all found in the vicinity of the aorta

Enteric Nervous System

• myenteric plexus: regulates gut smooth muscle; auerbach's
• submucous plexus: monitors chemcial and glandular secretion
• parasymp increases activity and sympathetic inhibits

Bara and chemo receptors

• barareceptors send information back along vagus 
• chemoreceptors in the carotid body send info back along glossopharyngeal IX
• reflexes can use inhibitory interneuron relays 
• high blood pressure causes a reduction of sympathetic activity in three places

Urination

• parasympathetic activation to contract bladder
• sympathetic inhibition to relax detrusor muscle and internal sphincter
• external sphincter opening(voluntary relaxation of tonically active input to striated sphincter muscle)
• stretch receptor in bladder wall activates and sends neuron up anterolateral system and synapses at periaqueductal grey (amygdala and hypothalamus also effects)
• periaqueductal grey sends it to pontine micturation center 
• this effects symp tone, activates parasympathetic neurons and ainhibitory local circuit neurons that then allow somatic motor neurons to fire

Sexual Function

• parasympathetic ns is responsible for arousal
• sympathetic ns is responsible for orgasm
• inferior mesenteric to the vas deferens
• parasymp to vas deferens and venous sinosoids (opens and allows erection)
• somatic motor (perineal muscles) and sensory receptors in genitals 

Sexual Function

Cortical input

• amygdala: execution and reward
• medial preoptic area: hypothalamus integrates hormone and sensory information
• hypothalamus: erection and lordosis
• hypothalamic nuclei: integrative center for sexual response, preference and gender identitiy
• thalamus: execution and reward
• bed nucleus of stria terminalis: execution and reward

Hypothalamic regions associated with

control of feeding

• arcuate nucleus: senses levels of leptin and at bottom of third ventricle: aMSH and CART-containing neurons stim by increased leptin
• paraventricular nucleus: associated with energy utilization
• lateral hypothalamus: associated with appetite(when activated increases appetite)
• arcuate nuclues sends input to both the other regions

Paraventricular nucleus

(hypothalamus)

• excited by αMSH and CART containing neurons
• increased secretion of CRH and TRH
• excitatory projection to brainstem and spinal cord sympathetic systems
• results: activate increased energy expenditure mechanisms
• inhibited by NPY and AGRP containg neurons, results in reduction in energy expenditure mechanisms

Lateral Hypothalamus

• inhibited by αMSH and CART containing neurons
• result: reduction of feeding behavior (anorexigenic)
• cells in here that contains MCH peptide that projects out to cortical areas (prefrontal) to control feeding behavior
• excited by NPY and AGRP containing neurons causing increased feeding behaviors (orexigenic effect)

Arcuate Nuc

(hypothalamus)

• αMSH and CART containing neurons stimulated by increased leptin
• NPY and AGRP containing neurons stimulated by decreased leptin levels
• these neurons effect both paraventricular nuc and lateral hypothalamus in opposite ways

Short term regulation of feeding

• orexigenic signals: ghrelin, smell of foods
• satiety signals: stomach distention, CCK, insulin, glucose
• orexigenic signals drop once you start feeding on a meal and satiety signals increase

Hypothalamus Mechanisms

of temperature regultion

• internal temp monitored in anterior hypothalamus
• cold sense neurons activate when body temperature dec, warm sense do oposite 
• set point located in medial preoptic term, recieve input from anterior hypothalamus and peripheral sensors
• heatloss mech is to increase sweating, and dilation of cutaneous blood vessels, and increase respiration, and reduce stimulation of thyroid and corticotropin hormones
• heat gain mechanisms include inc release of thyroid hormone, and visceral motor responses, activating shivering (a lot of these lateral hypothalamic)

Pyrogens

• have the affect of increasing body temp
• epithelial cells that are lining the hypothalamic cap beds, causes production of COX and PGF2, raising set point of body temp
• makes unfavorable environment for infectious things
• fever

Low Fluid balance in body

• organum vascularam of the lamina terminalis that senses the concetration of the blood (become active when Na concentration in blood is too high, sends signals to hypothalamus
• paraventricular and supraoptic nuc are h ypothalamic regions of fluid balance(release ADH into blood stream)
• dorsalmedial nuc of the hypothalamus sends neuron projections to cortex to promote drinking
• barareceptors send input through the solitary tract to hypothalamus when fluid low

Neurologic Exam 

Five Catagories

• mental status, speech, and language
• cranial nerves
• motor system
• sensory system
• reflexes

Cranial nerves III, IV, and VI

test

• pupillary reactions (edingerwestphal and CN II and III)
• identify nystagmus
• identify ptosis
• test extraocular movements