Anatomy and Physiology Flashcards

Question

Drugs that influence REM sleep

Answer 1

benzodiazepines, barbiturates and EtOH decrease REM and delta wave sleep; NE also decr REM sleep.

Answer 2

oral desmopressin acetate (DDAVP) mimics ADH; given to treat bedwetting (sleep enuresis) over imipramine because of the latter's adverse effects.

Answer 3

Benzodiazepines

Answer 4

Awake (eyes open): alert, active mental concentration Beta (highest frequency, lowest amplitude) Awake (eyes closed): Alpha Non-REM stage N1 (5%): light sleep Theta Non-REM stage N2 (45%): deeper sleep; bruxisms (teeth grinding) - sleep spindles and K complexes Non-REM stage N3 (25%): deepest non-REM sleep, when sleepwalking, night terrors, and bedwetting occur Delta (lowest frequency, highest amplitude REM sleep (25%): loss of motor tone, incr brain O2, incr variable pulse and BP; when dreaming and tumescence (erection) occur; may serve in memory processing Beta

Answer 5

Receives hypothalamic axonal projections from supraoptic (ADH) and paraventricular (oxytocin) nuclei (oxys= quick, tocos=birth) (adenohypophysis=anterior pituitary)

Answer 6

``` VPL: ventral posterolateral (body SS) VPM: ventral posteromedial (face SS) LGN: lateral geniculate nucleus (vision) MGN: medial geniculate nucleus (hearing) VL: ventral lateral (motor) ```

Answer 7

Ventral posterolateral nucleus of the thalamus: Input from spinothalamic (pain and temp) and dorsal column/medial lemniscus (pressure, touch, vibration, proprioception) to the primary somatosensory cortex.

Answer 8

Ventral posteromedial nucleus of the thalamus: | Input from trigeminal and gustatory pathway (face sensation and taste) to primary somatosensory cortex

Answer 9

Lateral geniculate nucleus of the thalamus: | Input from CN II (vision) to the calcarine sulcus (lateral=light)

Answer 10

Medial geniculate nucleus of the thalamus: Input from superior olive and inferior colliculus of tectum (hearing) to the auditory cortex of temporal lobe (medial=music)

Answer 11

Ventral lateral nucleus of the thalamus: | Input from basal ganglia, cerebellum (motor) to the motor cortex

Answer 12

Famous 5 F's (Feeding, Fleeing, Fighting, Feeling, Sex) Involved in emotion, long-term memory, olfaction, behavior modulation, ANS function. Includes hippocampus, amygdala, fornix, mammillary bodies, and cingulate gyrus. Critical for memory and motivation All areas receive rich monoaminergic and cholinergic innervation

Answer 13

Memory formation Patient H.M bilateral hippocampus lobectomy --> anterograde amnesia (no new memories) specifically explicit or declarative memory (facts/experiences) Not implicit memory (motor procedural skill) Hippocampus → mammillary bodies + branches to septal nuclei (via fornix)

Answer 14

Major role in fear conditioning Lesion prevents pavlovian conditioning to painful (fearful) stimuli Could play a role in PTSD Amygdala → septal nucleus (via stria terminalis)

Answer 15

Connects hippocampus to mammillary bodies + branches to septal nuclei (fibers over thalamus)

Answer 16

Mammillary body in thalamus → anterior nucleus of thalamus (via mammillothalamic tract) → cingulate gyrus + prefrontal cortex

Answer 17

Contralateral cortex via middle cerebellar peduncle. Ipsilateral proprioceptive information via inferior cerebellar peduncle from the spinal cord (nerves=climbing and mossy fibers)

Answer 18

Sends info to contralateral cortex to modulate movement. Nerves=purkinje cells -->deep nuclei of cerebellum --> contralateral cortex via superior cerebellar peduncle. Deep nuclei: Dentate, Emboliform, Globose, Fastigial (Don't eat greasy food)

Answer 19

Lateral hemispheres Cerebrocerebellum: reciprocal connections w/ cortex Spacially and temporally complex movements requiring coordination, cognition (learn complex movements) →contralateral VL thal→cortical motor areas →parvocellular red nucleus→ inferior olives→climbing fibers

Answer 20

Paravermis Spinocerebellum: appendicular movements (reaching, grasping) →VL thal→M1→lateral corticospinal tract →Magnocellular red nucleus→rubrospinal tract

Answer 21

Vestibulocerebellum

Answer 22

Vermis Spinocerebellar outputs: midline movements (speech, posture, stance, gait, visceral function) →superior cerebellar peduncle→VL thal→M1→ventral corticospinal tract →superior cerebellar peduncle→superior colliculus→tectospinal tract →inferior CP→reticular nuclei→reticulospinal tracts →inferior CP→vestibular nuclei→vestibulospinal tracts

Answer 23

Voluntary movements of extremities; when injured, propensity to fall toward injured (ipsilateral) side

Answer 24

Lesions of midline structures (vermal/fastigial nuclei) and/or the flocculonodular lobe result in truncal ataxia, nystagmus and head tilting. These patients also may have a wide-based (cerebellar) gate and deficits in truncal coordination. Generally, midline lesions result in bilateral motor deficits affecting axial and proximal limb musculature.

Answer 25

Important in voluntary movements and making postural adjustments. Receives cortical input, provides negative feedback to cortex to modulate movement. Striatum = putamen (motor) + caudate (cognitive) Lentiform = putamen + globus pallidus

Answer 26

Direct (D1 receptor) facilitates movement: Cortical inputs stimulate the striatum, stimulating the release of GABA which disinhibits the thalamus via the GPi/SNr (to incr motion) Dopamine binds to D1 stimulating the excitatory pathway (increasing motion) substantia nigra pars compacta (SNc) houses dopaminergic neurons that project to --> putamen (D1) where dopamine activates D1 receptors that --> inhibits globus pallidus internus (usually inhibits thalamus) which --> releases GPi inhibition of the thalamus so that --> thalamus can project motor signal to primary motor cortex

Answer 27

Indirect (D2 receptor) inhibits (unwanted) movement via: Cortical inputs stimulate the striatum, which disinhibits STN via GPe, and STN stimulates GPi/SNr to inhibit the thalamus (decreasing motion) Dopamine binds to D2, inhibiting the inhibitory pathway (increasing motion) substantia nigra pars compacta (SNc) houses dopaminergic neurons that project to --> putamen (D2) where dopamine inhibits D2 receptors (normally inhibit GPe) that --> releases inhibition of GPe so that it fires and inhibits sub thalamic nucleus) which --> no longer allows STN to fire and activate GPi --> so GPi then no longer inhibits the thalamus. (loss of inhibition of movement)

Answer 28

``` Degenerative disorder of CNS associated with Lewy bodies (composed of alpha-synuclein - intracellular eosinophiolic inclusion) and loss of dopaminergic neurons in substantial nigra pars compacta. Parkinson TRAPS your body: Tremor (at rest pill rolling) Rigidity (cogwheel) Akinesia (bradykinesia) Postural instability Shuffling gait ```

Answer 29

Autosomal dominant trinucleotide CAG repeats Chromosome 4 Loss of Ach and Gaba (CAG=Caudate loses Ach and Gaba) Symptoms manifest between 20-50 Chorea, aggression, depression, dementia Often accompanied by substance abuse (mistaken for) Neuronal death via NMDA-R binding and glutamate toxicity Atrophy of caudate nuclei seen on imaging

Answer 30

Sudden, wild flailing of 1 arm +/- ipsilateral leg | Lesion: contralateral subthalamic nucleus (eg lacunar stroke)

Answer 31

Sudden, jerky, purposeless movements | Lesion: basal ganglia (eg Huntington)

Answer 32

Slow, writhing movements' especially seen in fingers | Lesion: basal ganglia (eg Huntington)

Answer 33

Sudden, brief, uncontrolled muscle contraction | Notes: common in metabolic abnormalities such as renal failure and liver failure (e.g. jerks, hiccups)

Answer 34

Sustained, involuntary muscle contractions | Notes: Writers cramp;blepharospasm

Answer 35

Action tremor; exacerbated by holding posture/limb position Note: genetic predisposition. Patients often self-medicated with EtOH, which decr tremor amplitude Tx: beta-blockers, primidone

Answer 36

Uncontrolled movement of distal appendages (most noticeable in hands); tremor alleviated by intentional movement Lesion e.g. Parkinson disease Note: occurs at rest e.g. "pill rolling tremor"

Answer 37

Slow, zigzag motion when pointing/extending toward a target | Lesion: cerebellar dysfunction

Answer 38

Mossy fiber sensory/motor input info from spine, vestibular, auditory, visual info, proprioceptive from ipsilateral muscles excite deep cerebellar nuclei directly. Dorsal: sensory, clarke's nucleus, below C8 Ventral: motor info, ventral horn, below C8 Cuneocerebellar: sensory, cuneate nucleus, above C8 Rostral: motor info, ventral horn, above C8 Mesencephalic: nucleus face

Answer 39

"Climb the olive tree” (Contralateral Inferior olive → Climbing fibers→ Purkinje cell (looks like a tree)) “Moss on rock by pons” Mossy fiber going to granule (rock) from pontine nuclei (Pond sounds like pons)

Answer 40

Inferior: ipsilateral input from dorsal/rostral spinocerebellar, cuneocerebellar tracts Middle: massive contralateral input from pontine nuclei Superior: mostly output, input from ventral spinocerebellar tract

Answer 41

Wide, staggering gait, dysmetria, action tremor, timing disorders (dysdiadochokinesia), movement decomposition, inability to adapt motor programs

Answer 42

Problems w/ equilibrium and balance (fall toward side of lesion) Vertigo Visual problems (nystagmus, loss of smooth pursuit, diplopia)

Answer 43

``` Fine motor control deficits (writing) Highly skilled motions (speech, sports, instruments) Cognitive deficits (language deficits after PICA, behavioral) ```

Answer 44

Bilateral lesion of amygdala memory loss, new info with emotional content Impaired recognition of emotion in facial expression, inability to judge like emotions (fear vs anger)

Answer 45

Triad: Re-experiencing phenomena (flashbacks), avoidance of situations that parallel initial trauma, hyperarousal (hypervigilence) Promotes increase in anxiety Etiology: decrease inhibition of amygdala by prefrontal cortex, increase amygdala fear activity

Answer 46

Fragmentation of mood, thought, and movement (1% of population) Positive sxs: delusions, hallucinations Negative sxs: social withdrawal Tx: -dopamine hypothesis block DA receptors w/ Haloperidol. May see Parkinsonian-like side effects) -glutamate hypothesis block DA and 5-HT receptors + glutamate reuptake w/ clozapine

Answer 47

Bilateral medial temporal lobe damage (encephalitis, stroke) Sx: K - luver - bucy K: (okay) neutral affect luver: (lover) hypersexuality Gary bucy: (has a big mouth) visual agnosia - pt puts objects in mouth to identify

Answer 48

Etiology: loss of cholinergic input to hippocampus (nucleus basalis) Presence of neurofibrillary tangles (phosphorylated tau proteins) and beta-amyloid plaques Chronic progressive deterioration Loss of memory → mood disorders →loss of motor function → complete loss of cognitive function Tx: Donepezil (aricept): blocks ACh esterase → increase [ACh]

Answer 49

Progressive neurodegenerative disease caused by repeated head trauma Triad of sx: Cognition: memory impairment (anterograde), executive dysfx (goal-directed behaviors) Mood: depression, apathy Behavior: decreased impulse control, aggressiveness Etiology: generalized brain atrophy, NFTs present after exposure to multiple mild brain injuries or concussions.

Answer 50

Kluver-Bucy syndrome (hyperorality, hypersexuality, disinhibited behavior) Associated with HSV-1

Answer 51

Disinhibition and deficits in concentration, orientation, and judgment. May have reemergence of primitive reflexes

Answer 52

Rt: spatial neglect syndrome (agnosia of the contralateral side of the world) Lt: Agraphia, acalculia, finger agnosia, and left-right disorientation Gerstmann syndrome

Answer 53

Reduced levels of arousal and wakefulness (e.g. coma)

Answer 54

Wernicke-Korsakoff syndrome: Confusion, ophthalmoplegia, ataxia; memory loss (anterograde and retrograde amnesia), confabulation, personality changes Associated w/ thiamine (B1) deficiency and excessive EtOH use Can be precipitated by giving glucose without B1 to a B1-deficient patient (CAN of beer: Confusion, Ataxia, Nystagmus)

Answer 55

May result in tremor at rest, chorea, or athetosis (e.g. Parkinson)

Answer 56

Intention tremor, limb ataxia, and loss of balance Damage to cerebellum = ipsilateral deficits Fall toward side of lesion (Cerebellar hemispheres are laterally located - affect lateral limbs)

Answer 57

Trucal ataxia, dysarthria | Vermis is centrally located - affects central body

Answer 58

Contralateral hemiballismus

Answer 59

Anterograde amnesia (can't make new memories)

Answer 60

Eyes look away from side of lesion | Rt FEF --> Lt PPRF --> Lt CN VI --> Rt CN III (via MLF)

Answer 61

Eyes look toward lesion | Rt FEF --> Lt PPRF --> Lt CN VI --> Rt CN III (via MLF)

Answer 62

Osmotic demyelination; acute paralysis, dysarthria, dysphagia, diplopia, LOC Can cause "locked in syndrome" Massive demyelination of pontine white matter tracts 2/2 osmotic forces and edema. Commonly iatrogenic, overly rapid correction of hyponatremia (from low to high, your pons will die) -CPM Na+ correction (from high low low, your brain will blow) - cerebral edema/herniation

Answer 63

Aphasia: higher-order inability to speak (language deficit) Dysarthria: motor inability to speak (movement deficit)

Answer 64

Nonfluent aphasia with intact comprehension Broca area inferior frontal gyrus of frontal lobe (Broca boken boca - spanish)

Answer 65

Fluent aphasia with impaired comprehension and repition Wernicke area superior temporal gyrus of temporal lobe (Wernicke is Wordy but doesn't make sense)

Answer 66

Nonfluent aphasia with impaired comprehension. Both Broca and Wernicke areas affected

Answer 67

Poor repetition but fluent speech, intact comprehension. Can be caused by damage to left superior temporal lobe and/or left supra marginal gyrus (can't repeat phrases "no ifs, ands, or buts")

Answer 68

Nonfluent aphasia with good comprehension and repetition

Answer 69

Poor comprehension with fluent speech and repetition

Answer 70

Nonfluent speech, poor comprehension, good repetition

Answer 71

Rt brachiocephalic --> common--> Internal carotid Artery--> -Middle cerebral-->lenticulostriate/anterior choroidal -Anterior cerebral-->anterior communicating -Posterior communicating Sub-clavian --> Vertebral --> Basilar -Posterior Inferior Cerebellar -Anterior Spinal -Anterior Inferior Cerebellar -Superior cerebellar -Posterior cerebral

Answer 72

Anterior cerebral artery: anteromedial surface Middle cerebral artery: lateral surface Posterior cerebral artery: posterior and inferior surfaces Watershed zones between anterior/middle, posterior/middle artery zones. Damage in severe hypotension --> upper leg/upper arm weakness, defects in higher-order visual processing

Answer 73

Tight autoregulation primarily driven by PCO2 (PO2 also modulates perfusion in severe hypoxia <50mmHg) Therapeutic hyperventilation (decr PCO2) helps decrease intracranial pressure in cases of cerebral edema (stroke, trauma) via decreasing cerebral perfusion by vasoconstriction

Answer 74

Motor: Contralateral paralysis upper limb and face Sensory: Contralateral loss of sensation in upper/lower limb, face Temporal lobe (Wernicke)/Frontal lobe (Broca): Aphasia if in dominant (usually left) hemisphere. Hemineglect if lesion in non dominant.

Answer 75

Motor: contralateral paralysis lower limb Sensory: contralateral loss of sensation lower limb

Answer 76

Striatum, internal capsule: - contralateral hemiparesis/hemiplegia - common location of lacunar infarcts secondary to unmanaged hypertension

Answer 77

Commonly bilateral, Medial Medullary Syndrome Caused by infarct of paramedic branches of ASA and vertebral arteries. Lateral corticospinal tract: contralateral hemiparesis upper and lower limbs Medial lemniscus: decrease contralateral proprioception Caudal medulla(hypoglossal nerve): ipsilateral hypoglossal dysfunction (deviation ipsilaterally)

Answer 78

Lateral Medullary Syndrome (Wallenberg) -vestibular nuclei: Vomiting, vertigo, nystagmus; -lateral spinothalamic tract: pain and temperature sensation from contralateral body -spinal trigeminal nucleus: pain and temperature sensation from ipsilateral face -nucleus ambiguus: dysphagia, hoarseness, decr gag reflex -sympathetic fibers: ipsilateral Horner syndrome -inferior cerebellar peduncle: ataxia, dysmetria Nucleus ambiguus effects are specific to PICA lesions. “Don’t pick a (PICA) horse (hoarseness) that can’t eat (dysphagia).”

Answer 79

Lateral Pontine Syndrome—cranial nerve nuclei: -vestibular nuclei: vomiting, vertigo, nystagmus -facial nucleus: Paralysis of face, decr lacrimation, salivation, decr taste from anterior 2⁄3 of tongue -spinal trigeminal nucleus: decr corneal reflex, decr facial pain and temperature sensation. -cochlear nucleus: ipsilateral decr in hearing -sympathetic fibers: ipsilateral Horner syndrome -Middle and inferior cerebellar peduncles: ataxia, dysmetria Facial nucleus effects are specific to AICA lesions. “Facial droop means AICA’s pooped.”

Answer 80

Occipital cortex, visual cortex: contralateral hemianopia with macular sparing

Answer 81

"Locked-in syndrome" Pons, medulla, lower midbrain, corticospinal and corticobulbar tracts, ocular cranial nerve nuclei, paramedian pontine reticular formation: -Preserved consciousness and blinking, quadriplegia, loss of voluntary facial, mouth, and tongue movements

Answer 82

Most common lesion is aneurysm. Can lead to stroke. Saccular (berry) aneurysm can impinge cranial nerves. - Visual field defects - Lesions are typically aneurysms, not strokes.

Answer 83

Common site of saccular aneurysm. -CN III palsy—eye is “down and out” with ptosis and pupil dilation. -Lesions are typically aneurysms, not strokes.

Answer 84

-Occurs at the bifurcations in the circle of Willis -Most common site is junction of the anterior communicating artery and anterior cerebral artery. -Rupture (most common complication) leads to subarachnoid hemorrhage (“worst headache of life”) or hemorrhagic stroke. -Can also cause bitemporal hemianopia via compression of optic chiasm. -Associated with ADPKD, Ehlers-Danlos syndrome, and Marfan syndrome. -Other risk factors: advanced age, hypertension, smoking, race (incr risk in blacks).

Answer 85

``` Associated with chronic hypertension; affects small vessels (e.g., in basal ganglia, thalamus). ```

Answer 86

- Neuropathic pain due to thalamic lesions. - Initial sensation of numbness and tingling followed in weeks to months by allodynia (ordinarily painless stimuli cause pain) and dysaesthesia. - Occurs in 10% of stroke patients.

Answer 87

- Rupture of middle meningeal artery (branch of maxillary) - often 2° to fracture of temporal bone. - Lucid interval. - Rapid expansion under arterial pressure--> transtentorial herniation, CN III palsy. - CT shows biconvex (lentiform), hyper dense blood collection, not crossing suture lines. - Can cross falx, tentorium.

Answer 88

-Rupture of bridging veins. Slow venous bleeding -Seen in elderly, alcoholics, blunt trauma, shaken baby (predisposing factors: brain atrophy, shaking, whiplash). -Crescent-shaped hemorrhage that crosses suture lines -Midline shift. Cannot cross falx, tentorium

Answer 89

- Rupture of an aneurysm (berry aneurysm) - Patients complain of “worst headache of my life (WHOML).” -Seen in Marfan, Ehlers-Danlos, ADPKD) or an AVM. - Rapid time course. - Bloody or yellow (xanthochromic) spinal tap. - 2–3 days afterward, risk of vasospasm due to blood breakdown (not visible on CT, treat with nimodipine) and rebleed (visible on CT)

Answer 90

- Most commonly caused by systemic hypertension. - Also with amyloid angiopathy, vasculitis, and neoplasm. - Typically occurs in basal ganglia and internal capsule (Charcot-Bouchard aneurysm of lenticulostriate vessels), but can be lobar.

Answer 91

- Irreversible damage begins after 5 minutes of hypoxia. - risk: hippocampus, neocortex, cerebellum, watershed - Irreversible neuronal injury. Stroke imaging: Bright on diffusion-weighted MRI in 3–30 minutes (highest sensitivity for early ischemia), Dark abnormality on noncontrast CT in ~ 12–24 hours. Absence of bright areas on noncontrast CT highly accurate to exclude hemorrhage (contraindication for tPA).

Answer 92

``` Red neurons: 12-48 hours Necrosis + neutrophils: 24-72 hours Macrophages: 3-5 days Reactive gliosis+vascular proliferation: 1-2 weeks Glial scar: >2 weeks ```

Answer 93

- Intracerebral bleeding, often due to hypertension, anticoagulation, and cancer (abnormal vessels can bleed). --May be 2° to ischemic stroke followed by reperfusion (vessel fragility). - Basal ganglia are most common site of intracerebral hemorrhage.

Answer 94

- Disruption of blood flow and subsequent ischemia. - Results in liquefactive necrosis. 3 types: - Thrombotic—due to a clot forming directly at the site of infarction (commonly the MCA), usually over an atherosclerotic plaque. - Embolic—an embolus from another part of the body obstructs a vessel. Can affect multiple vascular territories. Often cardioembolic. - Hypoxic—due to hypoperfusion or hypoxemia. Common during cardiovascular surgeries, tends to affect watershed areas. Treatment—tPA (if within 3–4.5 hr of onset and no hemorrhage/risk of hemorrhage). Reduce risk with medical therapy (e.g., aspirin, clopidogrel); optimum control of blood pressure, blood sugars, and lipids; and treat conditions that incr risk (e.g., atrial fibrillation).

Answer 95

Brief, reversible episode of focal neurologic dysfunction lasting < 24 hours without acute infarction (neg MRI), with the majority resolving in < 15 minutes; deficits due to focal ischemia.

Answer 96

Large venous channels that run through the dura. Drain blood from cerebral veins and receive CSF from arachnoid granulations. Empty into internal jugular vein. Superior sagittal sinus, Inferior sagittal sinus, Straight, occipital sinus, confluence of the sinuses-->transverse-->sigmoid-->internal jugular vein

Answer 97

CSF is made by ependymal cells of choroid plexus; it is reabsorbed by arachnoid granulations and then drains into dural venous sinuses. Lateral ventricle --> 3rd ventricle via right and left interventricular foramina of Monro. 3rd ventricle-->4th ventricle via cerebral aqueduct (of Sylvius). 4th ventricle-->subarachnoid space via: -Foramina of Luschka = Lateral. -Foramen of Magendie = Medial.

Answer 98

Decreased Csf absorption by arachnoid granulations, which can lead to increased intracranial pressure, papilledema, and herniation (e.g. arachnoid scarring post-meningitis)

Answer 99

Does not result in increased subarachnoid space volume. Expansion of ventricles distorts the fibers of the corona radiata and leads to: clinical triad of urinary incontinence, ataxia, and cognitive dysfunction (sometimes reversible). “Wet, wobbly, and wacky.”

Answer 100

Appearance of increased CSF in atrophy (e.g., Alzheimer disease, advanced HIV, Pick disease). Intracranial pressure is normal; triad is not seen. Apparent increase in CSF observed on imaging is actually result of decreased neural tissue due to neuronal atrophy

Answer 101

Caused by a structural blockage of CSF circulation within the ventricular system (e.g., stenosis of the aqueduct of Sylvius).

Answer 102

There are 31 spinal nerves in total: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal Nerves C1–C7 exit above the corresponding vertebra. All other nerves exit below (e.g., C3 exits above the 3rd cervical vertebra; L2 exits below the 2nd lumbar vertebra).

Answer 103

nucleus pulpous (soft central disc) herniates through annulus fibrosus (outer ring); usually occurs posterolaterally at L4–L5 or L5–S1.

Answer 104

In adults, spinal cord extends to lower border of L1–L2 vertebrae. Subarachnoid space (which contains the CSF) extends to lower border of S2 vertebra. Lumbar puncture is usually performed between L3–L4 or L4–L5 (level of cauda equina) "To keep the cord alive, keep the spinal needle between L3 and L5."

Answer 105

Dorsal column/medial lemniscal pathway: pressure, vibration, touch, proprioception Fasciculus gracilis: lower body, legs (medial) Fasciculus cuneatus: upper body, arms (lateral) Lateral spinothalamic tract: pain, temperature Sacral (lateral) Cervical (medial) Anterior spinothalamic tract: crude touch, pressure)

Answer 106

Lateral corticospinal tract: voluntary motor (sacral lateral, cervical medial) Anterioir corticospinal tract: voluntary motor

Answer 107

Function: ascending pressure, vibration, fine touch, and proprioception. 1st neuron: Sensory nerve ending--> cell body in dorsal root ganglion-->enters spinal cord, ascends ipsilaterally in dorsal column Synapse 1: Ipsilateral nucleus cuneatus or gracilis (medulla) 2nd neuron: Decussates in medulla, ascends contra laterally in medial lemniscus Synapse 2: VPL thalamus 3rd neuron: Sensory cortex

Answer 108

Ascending Lateral: pain, temperature Anterior: crude touch, pressure 1st neuron: Sensory nerve ending (Aδ and C fibers) (cell body in dorsal root ganglion) -->enters spinal cord Synapse 1: Ipsilateral gray matter (spinal cord) 2nd neuron: Decussates at anterior white commissure -->ascends contra laterally Synapse 2: VPL thalamus 3rd neuron: Sensory cortex

Answer 109

Descending: voluntary movement of contralateral limbs 1st Neuron: UMN: cell body in 1° motor cortex-->descends ipsilaterally (through internal capsule), most fibers decussate at caudal medulla (pyramidal decussation)--> descends contralaterally Synapse 1: Cell body of anterior horn (spinal cord) 2nd Nueron: LMN: leaves spinal cord Snyapse 2: NMJ

Answer 110

Weakness, increased reflexes, increased tone, +babinski, spastic paralysis, clasp knife spasticity

Answer 111

Weakness, atrophy, fasiculations, decreased reflexes, decreased tone, (-) babinski, flaccid paralysis

Answer 112

Poliomyelitis and spinal muscular atrophy | LMN lesions only, due to destruction of anterior horns; flaccid paralysis

Answer 113

Combined UMN and LMN deficits with no sensory, cognitive, or oculomotor deficits; both UMN and LMN signs. Can be caused by defect in superoxide dismutase 1. Commonly presents as fasciculations with eventual atrophy and weakness of hands; fatal. Riluzole treatment modestly incr survival by decr presynaptic glutamate release. Commonly known as Lou Gehrig disease. Stephen Hawking is a well-known patient who highlights the lack of cognitive deficit. "For Lou Gehrig disease, give rilouzole."

Answer 114

Spares dorsal columns and Lissauer tract; upper thoracic ASA territory is a watershed area, as artery of Adamkiewicz supplies ASA below ∼T8.

Answer 115

Caused by 3° syphilis. Results from degeneration (demyelination) of dorsal columns and roots-->impaired sensation and proprioception and progressive sensory ataxia (inability to sense or feel the legs-->poor coordination). Associated with Charcot joints, shooting pain, Argyll Robertson pupils (small bilateral pupils that further constrict to accommodation and convergence, not to light). Exam will demonstrate absence of DTRs and +Romberg. "prostitutes pupil" - it accommodates but does not react

Answer 116

Syrinx expands and damages anterior white commissure of spinothalamic tract (2nd-order neurons)--> bilateral loss of pain and temperature sensation (usually C8–T1); seen with Chiari I malformation; can expand and affect other tracts.

Answer 117

Subacute combined degeneration—demyelination of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts; ataxic gait, paresthesia, impaired position and vibration sense.

Answer 118

Caused by poliovirus (fecal-oral transmission). Replicates in the oropharynx and small intestine before spreading via the bloodstream to the CNS. Infection causes destruction of cells in anterior horn of spinal cord (LMN death). Symptoms: LMN lesion signs—weakness, hypotonia, flaccid paralysis, fasciculations, hyporeflexia, and muscle atrophy. Signs of infection—malaise, headache, fever, nausea, etc. Findings: CSF with incr WBCs and slight incr of protein (with no change in CSF glucose). Virus recovered from stool or throat

Answer 119

Congenital degeneration of anterior horns of spinal cord -->LMN lesion. “Floppy baby” with marked hypotonia and tongue fasciculations. Infantile type has median age of death of 7 months. Autosomal recessive inheritance.

Answer 120

Autosomal recessive trinucleotide repeat disorder (GAA) on chromosome 9 in gene that encodes frataxin (iron binding protein). Leads to impairment in mitochondrial functioning. Degeneration of multiple spinal cord tracts-->muscle weakness and loss of DTRs, vibratory sense, and proprioception. Staggering gait, frequent falling, nystagmus, dysarthria, pes cavus, hammer toes, hypertrophic cardiomyopathy (cause of death). Presents in childhood with kyphoscoliosis. Friedreich is Fratastic (frataxin): he’s your favorite frat brother, always stumbling, staggering, and falling, but has a big heart.

Answer 121

Hemisection of spinal cord. Findings: - Ipsilateral UMN signs below the level of the lesion (due to corticospinal tract damage) - Ipsilateral loss of tactile, vibration, proprioception sense 1–2 levels below the level of the lesion (due to dorsal column damage) - Contralateral pain and temperature loss below the level of the lesion (due to spinothalamic tract damage) - Ipsilateral loss of all sensation at the level of the lesion - Ipsilateral LMN signs (e.g., flaccid paralysis) at the level of the lesion If lesion occurs above T1, patient may present with Horner syndrome due to damage of oculosympathetic pathway.

Answer 122

Sympathectomy of face: - Ptosis (slight drooping of eyelid: superior tarsal muscle) - Anhidrosis (absence of sweating) and flushing (rubor) of affected side of face - Miosis (pupil constriction) Associated with lesion of spinal cord above T1 (e.g., Pancoast tumor, Brown-Séquard syndrome [cord hemisection], late-stage syringomyelia). PAM is horny (Horner) Ptosis, Anhidrosis, Miosis The 3-neuron oculosympathetic pathway projects from the hypothalamus to the intermediolateral column of the spinal cord, then to the superior cervical (sympathetic) ganglion, and finally to the pupil, the smooth muscle of the eyelids, and the sweat glands of the forehead and face. Interruption of any of these pathways results in Horner syndrome.

Answer 123

C2—posterior half of a skull “cap.” C3—high turtleneck shirt. C4—low-collar shirt. T4—at the nipple. (T4 teat pore) T7—at the xiphoid process. T10—at the umbilicus (important for early appendicitis pain referral). (T10 belly butten) L1—at the inguinal ligament. (L1=IL-inguinal ligament) L4—includes the kneecaps. (down on AL L4's) S2, S3, S4—erection and sensation of penile and anal zones. (S2,3,4 keeps the penis off the floor) Diaphragm and gallbladder pain referred to the right shoulder via the phrenic nerve.

Answer 124

``` Achilles = S1 nerve root (S1,2 - buckle my shoe) Patella = L4 nerve root (L3,4 - kick the door) Biceps = C5 nerve root (C5,6 - pick up sticks) Triceps = C7 nerve root (C7,8 - lay them straight) ``` Also: L1,2 cremaster reflex (testicles move) S3,4 anal wink reflex (winks galore)

Answer 125

CNS reflexes that are present in a healthy infant, but are absent in a neurologically intact adult. Normally disappear within 1st year of life. These “primitive” reflexes are inhibited by a mature/ developing frontal lobe. They may reemerge in adults following frontal lobe lesions-->loss of inhibition of these reflexes. -Moro reflex: “Hang on for life” reflex—abduct/extend limbs when startled, and then draw together -Rooting reflex: Movement of head toward one side if cheek or mouth is stroked (nipple seeking) Sucking reflex: Sucking response when roof of mouth is touched Palmar reflex: Curling of fingers if palm is stroked Plantar reflex: Dorsiflexion of large toe and fanning of other toes with plantar stimulation Babinski sign: presence of this reflex in an adult, which may signify a UMN lesion Galant reflex: Stroking along one side of the spine while newborn is in ventral suspension (face down) causes lateral flexion of lower body toward stimulated side

Answer 126

``` CN I, II: forebrain CN III, IV: midbrain CN V: pons CN VI, VII, VIII: pons/pontine-medullary junction CN IX, X, XII: medulla CN XI: spinal cord ``` CN that lie medially in brain stem: III, IV, VI, XII Motor nerves are medial (medial nuclei= motor = basal plate) (lateral nuclei= sensory = alar plate)

Answer 127

Melatonin secretion, circadian rythms

Answer 128

Conjugate vertical gaze center Your eyes are above your ears, and the superior colliculus (visual) is above the inferior colliculus (auditory).

Answer 129

Auditory Your eyes are above your ears, and the superior colliculus (visual) is above the inferior colliculus (auditory).

Answer 130

Paralysis of conjugate vertical gaze due to lesion in superior colliculi (e.g., pinealoma)

Answer 131

``` I: olfactory II: optic III: oculomotor IV: trochlear V: trigeminal VI: abducens VII: facial VIII: vestibulochoclear IX: glossopharyngeal X: vagus XI: accessory XII: hypoglossal ``` "Some say mary money, but my bros say big boobs matter more" "Ooo, to touch and and feel very good velvet, ah ha"

Answer 132

I: olfactory: smell (only CN without thalamic relay to cortex) II: optic: sight III: oculomotor: Eye movement (SR, IR, MR, IO), pupillary constriction (sphincter pupillae: Edinger-Westphal nucleus, muscarinic receptors), accommodation, eyelid opening (levator palpebrae) IV: trochlear: Eye movement (SO) V: trigeminal: Mastication, facial sensation (ophthalmic, maxillary, mandibular divisions), somatosensation from anterior 2/3 of tongue VI: abducens: Eye movement (LR) VII: facial: Facial movement, taste from anterior 2/3 of tongue, lacrimation, salivation (submandibular and sublingual glands), eyelid closing (orbicularis oculi), stapedius muscle in ear (note: nerve courses through the parotid gland, but does not innervate it) VIII: vestibulochoclear: Hearing, balance IX: glossopharyngeal: Taste and somatosensation from posterior 1/3 of tongue, swallowing, salivation (parotid gland), monitoring carotid body and sinus chemo- and baroreceptors, and stylopharyngeus (elevates pharynx, larynx) X: vagus: Taste from epiglottic region, swallowing, soft palate elevation, midline uvula, talking, coughing, thoracoabdominal viscera, monitoring aortic arch chemo- and baroreceptors XI: accessory: Head turning, shoulder shrugging (SCM, trapezius) XII: hypoglossal: Tongue movement

Answer 133

Afferent: V1 ophthalmic (nasociliary branch) tirgeminal spinal nucleus-->bilateral facial nuclei--> Efferent: VII (temporal branch: orbicularis oculi)

Answer 134

Afferent: V1 (loss of reflex does not preclude emotional tears) Efferent: VII

Answer 135

Afferent: V3 (sensory - muscle spindle from masseter--> mesencephalic nuclus (only afferent system with primary cell bodies in the CNS)) Efferent: V3 (CNV motor nucleus --> masseter)

Answer 136

Afferent: CN II -->pretectal --> bilateral Edinger Westphal--> Efferent: CN III-->Ciliary ganglia-->pupillary sphincter

Answer 137

Afferent: IX Efferent: nucleus ambiguous --> X

Answer 138

Visceral Sensory information (e.g., taste, baroreceptors, gut distention). Input from: VII, IX, X

Answer 139

Motor innervation of pharynx, larynx, and upper esophagus (e.g., swallowing, palate elevation). Input from: IX, X, XI

Answer 140

``` Sends autonomic (parasympathetic) fibers to heart, lungs, and upper GI. Input from: X ```

Answer 141

Cribriform plate (CN I). Middle cranial fossa (CN II–VI)—through sphenoid bone: -Optic canal (CN II, ophthalmic artery, central retinal vein) -Superior orbital fissure (CN III, IV, V1, VI, ophthalmic vein, sympathetic fibers) -Foramen Rotundum (CN V2) -Foramen Ovale (CN V3) -Foramen spinosum (middle meningeal artery) Posterior cranial fossa (CN VII–XII)—through temporal or occipital bone: - Internal auditory meatus (CN VII, VIII) - Jugular foramen (CN IX, X, XI, jugular vein) - Hypoglossal canal (CN XII) - Foramen magnum (spinal roots of CN XI, brain stem, vertebral arteries) Divisions of CN V exit vis Standing Room Only

Answer 142

A collection of venous sinuses on either side of the pituitary. Blood from eye and superficial cortex-->cavernous sinus-->internal jugular vein. CN III, IV, V1, V2, and VI and postganglionic sympathetic fibers en route to the orbit all pass through the cavernous sinus. Cavernous portion of internal carotid artery is also here

Answer 143

e.g., due to mass effect, fistula, thrombosis: | ophthalmoplegia and decr corneal and maxillary sensation with normal visual acuity. CN VI commonly affected.

Answer 144

Jaw deviates toward side of lesion due to unopposed force from the opposite pterygoid muscle.

Answer 145

Uvula deviates away from side of lesion. Weak side collapses and uvula points away.

Answer 146

Weakness turning head to contralateral side of lesion (SCM). Shoulder droop on side of lesion (trapezius). The left SCM contracts to help turn the head to the right.

Answer 147

Tongue deviates toward side of lesion (“lick your wounds”) due to weakened tongue muscles on the affected side. Genioglossus protrudes tongue on contralateral side unopposed.

Answer 148

Visible portion of ear (pinna), includes auditory canal and eardrum. Transfers sound waves via vibration of eardrum.

Answer 149

Air-filled space with three bones called the ossicles (malleus, incus, stapes). Ossicles conduct and amplify sound from eardrum to inner ear.

Answer 150

Snail-shaped, fluid-filled cochlea. Contains basilar membrane that vibrates 2° to sound waves. Vibration transduced via specialized hair cells--> auditory nerve signaling--> brainstem. Each frequency leads to vibration at specific location on the basilar membrane (tonotopy): -Low frequency heard at apex near helicotrema (wide and flexible). -High frequency heard best at base of cochlea (thin and rigid).

Answer 151

Rinne: conductive hearing loss = bone>air Rinne: sensorineural hearing loss= air>bone Weber: Conductive localizes to affected ear Weber: Sensorineural localizes to unaffected ear Noise-induced: Damage to stereocilliated cells in organ of Corti; loss of high-frequency hearing 1st; sudden extremely loud noises can produce hearing loss due to tympanic membrane rupture.

Answer 152

Lesion of motor cortex or connection between cortex and facial nucleus. Contralateral paralysis of lower face Forehead spared due to bilateral UMN innervation.

Answer 153

Ipsilateral paralysis of upper and lower face.

Answer 154

Complete destruction of the facial nucleus itself or its branchial efferent fibers (facial nerve proper). Peripheral ipsilateral facial paralysis (drooping smile) with inability to close eye on involved side. Can occur idiopathically (called Bell palsy); gradual recovery in most cases. Associated with Lyme disease, herpes simplex and (less common) herpes zoster, sarcoidosis, tumors, and diabetes. Treatment includes corticosteroids

Answer 155

3 close jaw: Masseter, teMporalis, Medial pterygoid. 1 opens: lateral pterygoid. All are innervated by the trigeminal nerve (V3). M’s Munch. Lateral Lowers (when speaking of pterygoids with respect to jaw motion). “It takes more muscle to keep your mouth shut.”

Answer 156

Impaired vision that improves with glasses: Hyperopia: Eye too short for refractive power of cornea and lens-->light focused behind retina. Myopia Eye: too long for refractive power of cornea and lens-->light focused in front of retina. Astigmatism: Abnormal curvature of cornea resulting in different refractive power at different axes. Presbyopia: Decrease in focusing ability during accommodation due to sclerosis and decr elasticity.

Answer 157

Inflammation of anterior uvea and iris, with hypopyon (sterile pus), accompanied by conjunctival redness). Often associated with systemic inflammatory disorders (e.g., sarcoid, rheumatoid arthritis, juvenile idiopathic arthritis, TB, HLA-B27–associated conditions).

Answer 158

Retinal edema and necrosis leading to scar. Often viral (CMV, HSV, HZV). Associated with immunosuppression.

Answer 159

Acute, painless monocular vision loss. Retina cloudy with attenuated vessels and “cherry-red” spot at the fovea.

Answer 160

Blockage of central or branch retinal vein due to compression from nearby arterial atherosclerosis. Retinal hemorrhage and edema in affected area.

Answer 161

Retinal damage due to chronic hyperglycemia. Two types: Non-proliferative—damaged capillaries leak blood-->lipids and fluid seep into retina-->hemorrhages and macular edema. Treatment: blood sugar control, macular laser. Proliferative—chronic hypoxia results in new blood vessel formation with resultant traction on retina. Treatment: peripheral retinal photocoagulation, anti-VEGF injections.

Answer 162

Ciliary epithelium (beta) produces aqueous humor--> Flows through the posterior chamber (behind iris)--> Anterior chamber--> Trabecular meshwork--> Canal of Schlemm

Answer 163

Optic disc atrophy with characteristic cupping, usually with incr intraocular pressure (IOP) and progressive peripheral visual field loss.

Answer 164

Associated with age, African-American race, family history. Painless, more common in U.S. Primary—cause unclear. Secondary—blocked trabecular meshwork from WBCs (e.g., uveitis), RBCs (e.g., vitreous hemorrhage), retinal elements (e.g., retinal detachment).

Answer 165

Primary—enlargement or forward movement of lens against central iris (pupil margin) leads to obstruction of normal aqueous flow through pupil-->fluid builds up behind iris, pushing peripheral iris against cornea and impeding flow through trabecular meshwork. Secondary—hypoxia from retinal disease (e.g., diabetes, vein occlusion) induces vasoproliferation in iris that contracts angle. Chronic closure—often asymptomatic with damage to optic nerve and peripheral vision. Acute closure—true ophthalmic emergency. Incr IOP pushes iris forward--> angle closes abruptly. Very painful, sudden vision loss, halos around lights, rock-hard eye, frontal headache. Do not give epinephrine because of its mydriatic effect.

Answer 166

Painless, often bilateral, opacification of lens-->decr in vision. Risk factors: age, smoking, EtOH, excessive sunlight, prolonged corticosteroid use, classic galactosemia, galactokinase deficiency, diabetes (sorbitol), trauma, infection.

Answer 167

Optic disc swelling (usually bilateral) due to incr intracranial pressure (e.g., 2° to mass effect). Enlarged blind spot and elevated optic disc with blurred margins seen on fundoscopic exam

Answer 168

CN VI: lateral rectus (abducens) CN IV: superior oblique (trochlear) CN III: all the rest (SR, IR, MR, IO) The superior oblique abducts, intorts, and depresses while adducted.

Answer 169

eye looks down and out; ptosis, pupillary dilation, loss of accommodation

Answer 170

eye moves upward, particularly with contralateral gaze and head tilt toward the side of the lesion (problems going down stairs, may present with compensatory head tilt in the opposite direction).

Answer 171

medially directed eye that cannot abduct.

Answer 172

Constriction, parasympathetic: 1st neuron: Edinger-Westphal nucleus to ciliary ganglion via CN III 2nd neuron: short ciliary nerves to pupillary sphincter muscles

Answer 173

Dilation, sympathetic: - 1st neuron: hypothalamus to ciliospinal center of Budge (C8–T2) - 2nd neuron: exit at T1 to superior cervical ganglion (travels along cervical sympathetic chain near lung apex, subclavian vessels) - 3rd neuron: plexus along internal carotid, through cavernous sinus; enters orbit as long ciliary nerve to pupillary dilator muscles

Answer 174

Light in either retina sends a signal via CN II to pretectal nuclei in midbrain that activates bilateral Edinger-Westphal nuclei; pupils contract bilaterally (consensual reflex). Result: illumination of 1 eye results in bilateral pupillary constriction. Marcus Gunn pupil (afferent pupillary defect)—due to optic nerve damage or severe retinal injury. -bilateral pupillary constriction when light is shone in affected eye relative to unaffected eye. Tested with the “swinging flashlight test.”

Answer 175

CN III has both motor (central) and parasympathetic (peripheral) components. Motor output to ocular muscles—affected primarily by vascular disease (e.g., diabetes: glucose-->sorbitol) due to decr diffusion of oxygen and nutrients to the interior fibers from compromised vasculature that resides on outside of nerve. Signs: ptosis, “down and out” gaze. Parasympathetic output—fibers on the periphery are 1st affected by compression (e.g., posterior communicating artery aneurysm, uncal herniation). Signs: diminished or absent pupillary light reflex, “blown pupil” often with “down-and-out” gaze.

Answer 176

Separation of neurosensory layer of retina (photoreceptor layer with rods and cones) from outermost pigmented epithelium (normally shields excess light, supports retina)--> degeneration of photoreceptors-->vision loss. May be 2° to retinal breaks, diabetic traction, inflammatory effusions. Breaks more common in patients with high myopia and are often preceded by posterior vitreous detachment (flashes and floaters) and eventual monocular loss of vision like a “curtain drawn down.” Surgical emergency.

Answer 177

Degeneration of macula (central area of retina). Causes distortion (metamorphopsia) and eventual loss of central vision (scotomas). -Dry (nonexudative, > 80%)—deposition of yellowish extracellular material in and beneath Bruch membrane and retinal pigment epithelium (“drusen”) A with gradual decr in vision. Prevent progression with multivitamin and antioxidant supplements. -Wet (exudative, 10–15%)—rapid loss of vision due to bleeding 2° to choroidal neovascularization. Treat with anti-vascular endothelial growth factor injections (anti-VEGF) or laser.

Answer 178

Meyer loop—inferior retina; loops around inferior horn of lateral ventricle. Dorsal optic radiation—superior retina; takes shortest path via internal capsule. - Right anoxia (optic nerve lesion) - Bitemporal hemianopia (pituitary lesion, chiasm) - Left homonymous hemianopia (optic tract lesion) - Left upper quadratic anopia (right temporal lesion, MCA) - Left lower quadratic anopia (right parietal lesion, MCA) - Left hemianopia with macular sparing (PCA infarct), macula - -> bilateral projection to occiput - Central scotoma (macular degeneration) Note: When an image hits 1° visual cortex, it is upside down and left-right reversed.

Answer 179

Medial longitudinal fasciculus (MLF): pair of tracts that allows for crosstalk between CN VI and CN III nuclei. Coordinates both eyes to move in same horizontal direction. Highly myelinated (must communicate quickly so eyes move at same time). Lesions seen in patients with demyelination (e.g., multiple sclerosis). Lesion in MLF = INO: lack of communication such that when CN VI nucleus activates ipsilateral lateral rectus, contralateral CN III nucleus does not stimulate medial rectus to fire. Abducting eye gets nystagmus (CN VI overfires to stimulate CN III). Convergence normal. MLF in MS. When looking left, the left nucleus of CN VI fires, which contracts the left lateral rectus and stimulates the contralateral (right) nucleus of CN III via the right MLF to contract the right medial rectus. Directional term (e.g., right INO, left INO) refers to which eye is paralyzed.

Anatomy and Physiology Flashcards

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