Med Neuro

Front 1

General somatic sensory

Back 1

touch, pain, temp and proprioception of skin and muscle of head, neck and mouth. CN V, VII, IX-9, X-10

Front 2

Special Somatic Sensory

Back 2

Hearing and balance function in cochlea+vestibular organs. CN VIII-8.

Front 3

Special visceral sensory

Back 3

vision, taste and olfaction in eyes, taste buds,an olfactory skin. CN I, II, VII, IX, X.

Front 4

General Somatic Motor

Back 4

skeletal muscle control to eye an tongue muscles. CN III, IV-4, VI-6, XII-12. Also to face, jaw, neck, throat, tongue. CN V, VII, IX-9, X, XI-11.

Front 5

General visceral sensory

Back 5

Mechano+chemo sensation in neck, throat, tongue.

CN III, VII, IX, X

Front 6

General visceral motor

Back 6

func: autonomic efferents. At pupils, tear, salivary, throat and abdomen. CN III, VII, IX, X.

Front 7

Diplopia

Back 7

Double vision (CN III oculomotor nerve and IV-4 trochlear nerves deficit) and close vision focus problems.

Front 8

3rd nerve palsy

Back 8

(Oculomotor CN III deficit) Loss of inward, upward and downward movement.

Front 9

CN V (5)-Opthalmic v1

Back 9

largest of cranial nerves-Trigeminal nerve-Opthalmic V1: function-sensations from anterior (front) scalp, eyelids and nose. Clinical test: corneal blink test (involuntary blinking when object nears). Deficit: trigeminal neuralgia.

Front 10

CN VIII (8)

Back 10

vestibular-Assesses position of body in space (equilibrium). Dorsal and ventral- Conveys auditory information to cochlea.Clinal test: hearing with tuning fork, balance and temp testing. Deficit- deafness and tinnitus (ringing in ears) and dizziness, loss of balance, nausea. Also nystagmus-REM (rapid eye move in sleep) from loss of reflex control of extraocular muscles.

Front 11

CN XII (12)

Back 11

hypoglossal nerves-tongue. sensory func: movement of in+extrinsic tongue muscles. motor-controls tongue muscles during chewing, swallowing+speech. clinical test: protrude and retract tongue. deficit-12th nerve palsy-swallowing+speech trouble, bilateral lesion-no protrusion, uni-tongue deviates to lesion side at rest or moving, possible atrophy (waste away).

Front 12

CN IV (4)

Back 12

trochlear nerves- Sensory function: proprioception from superior oblique mus. Motor: control of superior oblique mus. Clinical testing: pupil size, shape, light reflex, convergence + following object movement. Deficit: 4th nerve palsy-reduced ability to rotate eye down to one side (inferolaterally). Internal strab-inferior medial rotation at rest. Diplopia.

Front 13

CN IX (9)

Back 13

Glossopharynheal nerves- throat. Sensory-proprioception and touch from pharynx muscles and posterior 1/3 tongue, taste of back tongue. motor-pharynx muscles for swallowing. auto-parasympathetic control of parotid salivary gland. baroreceptors (blood vessel receptors) in carotid sinus for bp. Clinical test-uvula position, swallow+gag, taste in back 1/3, speech+cough.

Front 14

CN XI (11)

Back 14

accessory nerves-neck muscles. sensory func: movement of neck and shoulders. motor-control of neck, shoulder,+ throat muscles. clinical test: muscle strength by head rotation and shoulder shrugs. deficit- 11th nerve palsy-head rotation towards paralyzed neck muscles+unilateral should droop, shrug difficulty.

Front 15

CN X (10)

Back 15

Vagus-sensory-visceral impulses form throat, heat, lungs, kidneys, and digestive organs. motor+auto-motor throat, para-control hr, resp, digestion. clinical test-uvula position, swallow+gag reflex, speech an cough, baroreflex of bp and hr. Deficits-bulbar: voice production (dysarthria)+swallowing(dysphagia), loss of gag reflex. High bp, hr, resp.

Front 16

CN VII

Back 16

Facial Nerves: sensory function-proprioception of facial muscles of expression, taste impulses of frontal 2/3 tongue (sweet and salty). Motor-muscles of expression. autonomic-parasympathetic control of lacrimal (tears) +salivary glands. clinical testing-taste on frontal 2/3 tongue, face muscle symmetry, face expression-whistle, smile, tear w/ ammonia.

Front 17

Cranial Nerves

Back 17

Smell (I), Vision (II), Eye movement (III, IV-4, VI-6), Facial sensation (V-5), Facial expression (VII-7), Hearing and balance (VIII-8), Oral sensation, taste, and salivation (IX-9), Vagus nerve (X-10) (uvula, hoarse voice, raised hr +bp), Shoulder elevation and head-turning (XI-11), Tongue movement (XII-12).

Front 18

CN I

Back 18

Olfactory Nerves (under frontal lobe)

Clinical testing: Sniff and identify aromantic substances (vanilla). Deficit is Anosmia (loss of smell), bilaterally-mucous membrane (cold), unilaterally- fiber lesions or ethmoid bone fracture

Front 19

CN II

Back 19

Optic Nerves (Vision)

Clinical Testing-visual field tests, opthalmoscope assessment of optic disc and vasculature. Deficit- Anopias (visual field deficit), nerve-ipsilateral blindness. chasm-bitemporal hemianopia. optic tract- contralateral homonymous hemianopia. Optic radiation- contralateral hom. hem. (full)

Front 20

Anosmia

Back 20

loss of smell

Front 21

anopias

Back 21

visual field deficits

Front 22

ipsilateral

Back 22

lesion affects same side of body

Front 23

contralateral

Back 23

Lesion affects opposite side of the body

Front 24

bitemporal hemianopia

Back 24

partial blindness where vision is missing in the outer half of both the right and left visual field.

Front 25

Contralateral homonymous hemianopia

Back 25

-Hemianopia is visual field loss (lesion affects opposite side of the body) of the vertical midline (only see right side of things).

-Homonymous hemianopia, is hemianopic visual field loss on the same side of both eyes.

Partial= optic tract deficit, full=optic radiation.

Front 26

CN III

Back 26

Oculomotor nerve- function: Sensory-4 extrinsic eye muscles-inferior, oblique +superior and inferior+medial rectus. Motor-direct 4 eye muscles for eye movement (raise eyelid-levator palpebrae). Autonomic-pupil constriction and lens control. Clinical testing: pupil size, shape, reflex, convergence and following object. Deficit: 3rd nerve palsy-loss of inward, upward and down

Front 27

CN III (continued)

Back 27

movement. External strabismus: lateral rotation at rest (exotropia) -one eye goes to side while other is straight). Ptosis- eyelid droop. Diplopia: double vision+ close vision focus problems.

Front 28

external strabismus

Back 28

CN III deficit (extropia)

Front 29

ptosis

Back 29

eyelid droop (CN III oculomotor deficit)

Front 30

4th nerve palsy

Back 30

reduced ability to rotate eyes inferolaterally (down to one side) (CN IV trochlear deficit).

Front 31

Internal strabismus

Back 31

One eye turns inward while other is straight (CN IV trochlear deficit).

Front 32

CN V (5) Maxillary v2

Back 32

functions: sensation from cavity, palate, teeth, lips and cheeks. Clinical testing: site pain and temp tests. Deficit: trigeminal neuralgia.

Front 33

CN V Mandibular v3

Back 33

sensation from ant (frontal) tongue, lower teeth, chin and motor to mastication muscles. Clinical tests: site pain and temp tests, motor-teeth clench and jaw movement. Deficit: trigeminal neur.

Front 34

trigeminal neuralgia

Back 34

Pressure on nerve roots causing stabbing pain, triggered by mild sensory input (teeth brushing, wind on face) to v2 and v3 regions. treatment would be to cut nerve and stop all sensation from ipsilateral (same side) side of face.

Front 35

CN VI-6 abducens nerves

Back 35

sensory function: proprioception from lateral rectus muscle (back eye). motor-control of lateral rectus muscle. clinical test: pupil size, shape, light reflex, convergence and following object movement. Deficit: 6th nerve palsy-esotrpia-one eye moves inward. internal strabismus-estropia.

Front 36

6th nerve palsy

Back 36

deficit in VI-one eyes moves inward-estropia.

Front 37

CN VII Deficit- Bell's Palsy

Back 37

Facial muscle paralysis likely on one side, lower eye droop, mouth corner sag, uncontrolled tearing. May be caused by herpes or lyme disease that produces nerve inflammation.

Front 38

Nystagmus

Back 38

REM (rapid eye movement in sleep) from loss of reflex control of extraocular muscles. Deficit to VIII inner ear CN.

Front 39

Tinnitus

Back 39

Ringing in ear-deficit to VIII CN inner ear

Front 40

CN IX-9 deficit-bulbar dysphagia

Back 40

Deficit- bulbar dysphagia- trouble swallowing and taste (bitter), loss of gag reflex.

Front 41

dysarthria

Back 41

coarse voice CN IX-9 deficit, ALS Sign.

Front 42

dysphagia

Back 42

trouble swallowing CN IX-9 Deficit, ALS Sign.

Front 43

11th nerve palsy

Back 43

head rotation towards paralyzed neck muscles+unilateral should droop, shrug difficulty.

Front 44

12th nerve palsy

Back 44

swallowing+speech trouble, bilateral lesion-no protrusion, uni-tongue deviates to lesion side at rest or moving, possible atrophy (waste away).

Front 45

MS Etiology

Back 45

Genetic and autoimmune disease resulting in CNS demyelination (damage to sheath of neuron: limits signaling). Scar tissue replaces myelin. Ascending sensory and descending motor CNS fibers affected; peripheral nerves spared. The action propagation is reduced and ultimately ceases.

Front 46

MS Diagnosis

Back 46

Signs of disease in different parts of nervous system and signs of at least two separate relapses.

Front 47

MS Diagnostic tests

Back 47

MRI: white matter plaques develop, extend from damson's fingers (/ in center brain). Neurologic exam: reflexes, balance, coordination, vision and sensory deficits. Evoked potentials: EEG responses to sensory stimuli-visual, auditory and peripheral touch (light breeze, from clothes). Spinal tap: oligodendrocyte fragments in CSF.

Front 48

MS signs and Symptoms

Back 48

fatigue: muscle weakness leads to gait problems, UMN lesions, internal capsule. motor dysfunction: ataxia from damage to cerebellum tracts, spastic paralysis, nystagmus- brain stem or cerebellar. sensory impairments: vibratory and position sense, pain, temp, and touch impaired, vision deficits (optic neuritis). autonomic: bladder and bowel dysfunction

Front 49

ataxia

Back 49

lack of voluntary coordination of muscle movements such as walking or picking up objects-> sign of MS.

Front 50

Nystagmus

Back 50

involuntary eye movement-> sign of MS

Front 51

spastic paralysis

Back 51

persistent spasms and exaggerated tendon reflexes -> sign of MS

Front 52

optic neuritis

Back 52

inflammation of the optic nerve causing eye pair and/or visual loss-> sign of MS.

Front 53

MS Categories

Back 53

4 clinical courses (all can be mild, moderate or severe). Relapsing/remitting: (85% freq) clearly defined relapses of symptoms followed by partial or complete RECOVERY PERIODS FREE OF DISEASE PROGRESSION. Primary progressive: (10%) SLOW BUT CONTINUOUS worsening of disease from onset, no district relapses or remissions, varies in rates of profession.

Front 54

MS Categories (continued)

Back 54

Secondary progressive: (50% w/ RR develop within 10 yrs) initial period of RR FOLLOWED BY WORSENING DISEASE course with or without RR. Progressive relapsing: (5%) steadily worsening disease with clear acute relapses, with or w/o recovery. Periods between RELAPSES ARE CHARACTERIZED BY CONTINUING DISEASE PROGRESSION.

Front 55

MS Treatments

Back 55

High dose steroids-anti inflamatory. Interferon: inhibit inflamatory cytokines and monocytes. Copaxone: convert T cells to anti-inflamatory agents. Fampridine: blocks voltage gated potassium channels (block return to resting in action potentional).

Front 56

ALS Etiology

Back 56

Idiopathic progressive degeneration of Upper and lower motor neurons- excitotoxicity (nerve cells damaged and killed by over stimulation) +oxidative stress (antioxidants not stopping free radicals killing cells+mutating genes). Leads to resp failure and death in 23-52 yrs. Starts with focal (coordination, spine and talking) motor signs and spreads to muscle groups.

Front 57

ALS Signs and Symptoms

Back 57

Bulbar complaints: dysarthria: motor speech deficit. Dysphagia: swallowing deficit. General motor dysfunction: UMN-increased tone and hyper-reflexia, LMN atrophy and fasculations. Bilateral paresis w/ head drop, extrocular muscles spared. Pseduobulbar affect:uncontrolled laughter or crying w/o accompanying emotions.

Front 58

Hyper-reflexia

Back 58

overactive or over responsive reflexes-twitching or spastic, sign of UMN ALS.

Front 59

Atrophy

Back 59

body or tissue waste away, due to cell degeneration, sign of LMN ALS.

Front 60

Fasculations

Back 60

muscle twitch, LMN ALS sign.

Front 61

extraocular muscles

Back 61

Muscles that move the eye -> sign of ALS

Front 62

paresis

Back 62

weakness of voluntary movement-> ALS sign

Front 63

pseudobulbar affect

Back 63

uncontrolled laughter or crying without accompanying emotions-> ALS Sign.

Front 64

ALS Treatments

Back 64

Rilutek/ Riluzole: Na+, Ca+ and NMDA-R channel blockade. Ceftriaxone: IV antibiotic reduce excitotoxiciy in motor neurons. Tamoxifen: estrogen receptor antagonist.

Front 65

Unilateral Face, Arm and Leg paresis+ataxia with no sensory deficits

Back 65

Lesion location-contralateral corticospinal tracts below cortex and above medulla. Causes: internal capsule infarct, pons infarct, tumor, demyelination in same areas. Features: Dysarthria (speech problem) and unilateral ataxia (lack of voluntary coordination).

Front 66

Unilateral face, arm, and leg with sensory deficits

Back 66

lesion location: contralateral primary motor cortex, corticospinal tracts below cortex and above medulla. Causes: infarct hemorrhage, trauma, tumor, post-ictal state (seizures). Features: somatosensory, oculomotor and visual deficits, aphasia (comprehension and expression of lang), ataxia contra laterally, neglect.

Front 67

aphasia

Back 67

difficulty comprehending and expressing language-> feature of unilateral face, arm and leg with sensory deficits in primary motor cortex.

Front 68

hemiparesis sparing face

Back 68

lesion location: contralateral primary motor cortex or medulla (above pyramidal decuss), IPSILATERAL CERVICAL SPINAL CORD. Causes: watershed infarct, medullary infarct. Features: proximal muscles affected, vibration and joint position loss. Spinal cord-ipsilateral weakness+vibration and contralateral pain and temp loss.

Front 69

Brown-Sequard Syndrome

Back 69

Spinal cord feature of hemiparesis sparing face and lesion to cervical spinal cord and motor cortex above medulla- ipsilateral weakness+vibration and contralateral pain and temp loss.

Front 70

unilateral face and arm

Back 70

lesion location: contralateral primary motor cortex and arm and face regions. Causes: MCA infarct, tumor, demyelination in same areas. Features: dysarthria (speech), dominant hemisphere-brocas aphasia, non dominant hems-hemineglect, possible contralateral sensory loss.

Front 71

brocas aphasia

Back 71

good comprehension, non-fluent response, missing words in sentences giving confusing responses. Associated with lesion to primary motor cortex and causing unilateral face and arm paresis.

Front 72

hemi-neglect

Back 72

unilateral neglect-occurs in non dominant hemisphere with primary motor cortex lesion and paresis of unilateral face and arm.

Front 73

bilateral arm and leg

Back 73

lesion location-bilateral primary motor cortex, bilateral medullary corticospinal tracts. Causes: bilateral watershed infarct, medulla/spinal cord tumor, tramua. Features: aphasia, neglect, sensory loss, autonomic dysfunction, resp weakness, tongue weakness.

Front 74

bilateral arm

Back 74

lesion location: cervical cord. Causes: tumor, trauma. Features: bilateral somatosensory loss with pain and temp.

Front 75

bilateral leg

Back 75

lesion location: bilateral primary motor ctx, spinal cord thoracic and lumbar. Causes: meningioma, tumor, trauma. Features: frontal lobe dysfunction, confusion, apathy, grasp reflexes, autonomic dysfunction, reflex loss.

Front 76

Cerebellar Ataxia

Back 76

lesions to cerebellar produce ipsilateral deficits.

Front 77

Cerebellar truncal ataxia

Back 77

lesion in vermis- wide-based, unsteady gait, difficulty sitting w/o support in severe cases.

Front 78

cerebellar appendicular ataxia

Back 78

lesion in lateral hemisphere. Abnormal movements in extremeties, dysmetric-under or overshoot of target. common features- postural tremor, head and trunk tremor, nystagmus (uncontrolled eye movement).

Front 79

dysmetric

Back 79

under or overshoot of target (ocular)

Front 80

parkinsons etiology

Back 80

Idiopathic PD: degeneration in dopaminergic substantia nigra neurons, loss of corpus striatal dopamine hypersensitizes receptors. Iatrogenic Parkinsonism: anti-psycotic meds block striatal receptors. Atherosclerotic parkinsonism: increased risk in elderly hypertensives (high BP). Surviving nerve cells show lewy bodies (ab aggregates of protein inside nerve cells).

Front 81

basal ganglia and Parkinson's

Back 81

Striatum=caudate and putamen nuclei that received dopaminergic inputs. Within striatum-> Globus pallidus= large inhibitory input to thalamic ventral nucleus. PD associated with reduced GP inhibition that disinhibits the thalamus and increases excitation to the pre-motor CTX (SMA). GP doesn't inhibit and over stimulation occurs to premotor CTX.

Front 82

PD Signs

Back 82

tremor-alternating contraction of agonists and antagonists DURING RESTING PERIODS. Rigidty- plastic: resistance to passive movement, tremor absent. cogwheel:jerking movements, tremor present. Bradykinesia: slow movements, expressionless face, arm swinging absent during walking. postural disturbances- standing with forward flex of trunk and arms-retropulsion.

Front 83

bradykinesia

Back 83

PD Sign- slow movements, expressionless face, arm-swinging during walking absent.

Front 84

PD Signs (continued)

Back 84

hypo phonic speech-monotone, fast and slurred. mircrographia-small writing font size. myersons sign-continual blink test. normal muscle strength, sensory systems, deep tendon reflexes.

Front 85

T2 vs T1 MRI

Back 85

T2-Black bone, hypointencity black. T1- white bone, hyperintensity white. CT less detailed images. PET-colorful.

Front 86

PD Treatments

Back 86

medical- dopamine precursors: levadopa, MAO-B inhibitors. Surgical-deep brain stimulation of thalamus and sub thalamic nuclei, basal ganglia lesions. Tissue transplant: dopamine producing stem cells.

Front 87

sensory neurons

Back 87

the larger in diameter, the faster action potential propagation. Reside in dorsal root ganglion.

Front 88

touch and vibration pathway

Back 88

posterior column-medial lemniscus, ascends in spinal cord posterior column

Front 89

pain and temp pathways

Back 89

anterolateral-spinothalamic

Front 90

somatosensory CTX

Back 90

primary-recieve thalamic sensory neuron signaling location and intensity.

soma association ctx- posterior parietal ctx enhances perception qulaities

Front 91

sensory loss patterns- primary soma ctx and thalamic lesion

Back 91

deficit is contralateral to lesion site. lesion size dictates size of decitit location and intensity. touch and joint position sense reduced often, excitation and graphesthesia (recognize writing on skin) present. UMN paresis, visual field deficits, aphasia (no comp or express of lang).

Front 92

sensory loss patterns- lateral pontine or medullary lesion

Back 92

anterolateral-contralateral body temp and pain loss, hemiparesis, dysarthria (hoarseness) and dysphagia (swallowing).