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Neurology Flashcards

1
Q

How do neurochord defects formed?

A

Neuropores fail to fuse in 4th week
Have persistant connection between amniotic cavity and spinal canal

Associated with low folic acid intake before the contraception and during the pregnancy

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2
Q

How to diagnose neural tube defects?

A

Increased alpha fetoprotein

Increase acetylycholinesterase in amniotic

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3
Q

What is spina bifida occulta?

A

Failute of bony spinal canal to close (no herniation)
Usually at the lower vertebral levels
Dura is intact
Associayed with a tuft of hair or skin dimple at the level of bony effect

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4
Q

Meningocele?

A

Meniniges (but no neural tissue) herniates through the bony defect

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5
Q

Meningomyelocele?

A

Meninges and neural tissue herniate through the bony defect

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6
Q

Anencephaly?

A

Malformation of anterior neural tube (no forbrain, empty calvarium)

Increase AFP
Polyhydraminos
Associated with maternal type 1 diabetes
No swallowing center of the brain

Forebrain

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7
Q

Holoprosencephaly?

A

Failure of the right and left hemisphere to seperate
Usually occurs during 5-6

Forebrain

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8
Q

Chairi II malformations?

A

Herniation of low lying cerebeller vermis through the foramon mangnum

Causes hydrocephalus

Associated with lumbrosacral meninogmyelocele

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9
Q

Dandy-Walker syndrome?

A

Agenesis of the cerebellar vermis with cystic enlargement of the 4th ventricles

Enlarged posterior Fossa

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10
Q

Syringomyelia?

A

Cystic cavity (syrinx) within the central canal
Fibers crossing anterior white commissure are damaged first
Have cape-like bilateral loss of pain and temperature sensation in the upper extremities

Manifestations: Bilateral loss of pain and temperature sensation in the upper extremities

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11
Q

What is Chiari I malformation?

A

Cerebeller tonsillar ectopia (between 3-5mm) cengential, assymptomatic in childhood.

Manifests with headache and cerebellar symptoms

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12
Q

What are nerves of the tongue?
Taste
Pain
Motor

A

Taste: CN VII, IX, X
Pain: CN V3, IX, X
Motor: CN X, XII

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13
Q

What are neurons?

A

Signal transmitting cells of the nervous system
Permanent cells (do not divide in adulthood)
Have signal relaying dendrites (receive input) cell bodies, axons send cell output

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14
Q

What happens when there is an injury to the axon ?

A

Have degeneration distal to the injury and axonal retraction

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15
Q

What is the function of astrocytes?

A 
Physical support
Repair
K metobolism 
Removal excess neurotransmitter 
Compoenent of blood brain barrier
Glycogen fuel reserve buffer
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16
Q

what is a microglia

A

Are scavenger cells within the CNS

in HIV fuse to form multinucleated giant cells in CNS

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17
Q

What are Myelin cells?

A

Increase conduction of velocity signals transmitted down axons

Saltatory conduction of action potentials at the nodes of Ranvier

(High concentration of Na+ channels), oligodendrocytes

Wraps and insulates the axon

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18
Q

What are Schwann cells?

A

Each Schwann cell myelinated only 1 PNS neuron
Promotes axonal regeneration
Increases condution velocity via saltatory conduction at the nodes of Ranvier

There is a high concentration of Na+ channels

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19
Q

What are oligodendroglia?

A 
Myleinates axons of neurons in CNS 
Predominate type of glial cell 
Derived from neuroectoderm 
Fried egg appearance 
Injured in multifocal leuckoencephalopathy
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20
Q

Free nerve endings?

A

C-slow unmyelinated fibers
A gamma- fast myelinated fibers

Location: all skin, epidermis with some viscera

Senses pain, temperature

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21
Q

Meissner corpuscles?

A

Large, myelinated fibers adapt quickly
Location: deep skin layers and ligament joints
Respond to vibration and pressure

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22
Q

Pacinian corpuscles?

A

Large myelinated fibers (adapt quickly)
Deep skin layers, ligaments and joints
Respond to vibration and pressure

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23
Q

Merkel disks?

A

Large myelinated fibers adapt slowly

Location: finger tips, superficial skin

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24
Q

Ruffani corpuscles?

A

Dendritic endings with capsule
Adapt slowly
Fingertips and joints
Senses: Pressure slippage of objects along the skin surface

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25
Q

What are portions of the peripheral nerves?

A

Endoneurium: single nerve fiber layers

Perineurium: surrounds the fascicle nerve fibers
Must be rejoined in microsurgery of the limp

Epineurium:
Dense Connective tissue that surrounds the entire nerve (fascicles and blood vessels)

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26
Q

Where are the following neurotransmittors found?

What happens in their clinical diseases?

A

Acetylcholine (Basal nucleus Meynett)
Alzeihmer’s disease: decrease
Huntington’s disease: decrease
Parkinson’s disease: increase

Dopamine: (Ventral tegmentun SNCP) 
Depression: decrease
Schizophrenia increase
Huntington: Increase
Parkinson: decrease

GABA (nucleus accumbens): decrease anxiety, decrease huntingtons

Norepinephrine: (locus ceruleus)
Increase in anxiety
Decrease in depression

Serotonin (raphe nucleus)
Decrease in anxiety
Decrease in depression
Increase in Parkinsons

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27
Q

Functions of the hypothalamus?

A

Thirst and water balance
Adenohypophysis (regulates anterior pituitary)
Neurohypophysis:
Hunger
Autonomic regulation Temperature regulation
Sexual urges

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28
Q

What does the lateral area do?

A

Hunger

destruction will lead to anorexia

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29
Q

Function ventromedial area?

A

Satiety Destruction (craniopharyngioma)

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30
Q

Function of anterior hypothalamus?

A

cooling

parasympathetic

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31
Q

Function of posterior hypothalamus?

A

Heating

Sympathetic

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32
Q

Function of suprachiasmatic nucleus?

A

Circadian rhythm

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33
Q

What controls sleep?

A

Circadian rhythm (by the supracharismatic nucleus)

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34
Q

What hormones are released by nocturnal controls?

A

Norepinephrine, pineal gland, melatonin,

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35
Q

What are the stages of sleep physiology?

A

REM and non REM

REM occurs every 90 minutes and duration of REM increases with release of ACh

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36
Q

What substances are associated with decrease REM?

A

ETOH, benzo, barbiturates

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37
Q

How to treat bedwetting?

A

Sleep enuresis, treated with desmopressin (ADH analog) preferred over imipramine

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38
Q

What medication is useful for night terrors and sleep walking?

A

Benzodiazepines

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39
Q

What are the ECG waveforms for the different stages of sleep?A

A

Awake (eyes open, alery, active mental concentration) Beta waves

Awake (eyes closed) alpha

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40
Q

What are stages of NON-REM sleep?

A

N1 (5%) light sleep (theta)
N2 (45%) deeper sleep when bruxism occurs (sleep spindles and K complexes)
N3 (25%) Deepest non REM sleep (slow wave) when sleepwalking, night terrors, and bed wetting

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41
Q

What is REM sleep?

A 
Loss of motor tone
Increase in O2 use
Variable pulse pressure
Penile and clitoral tumescence
May serve memory
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42
Q

Use of Ventral postero-lateral nucleus ?

A

Input: spinothalamic and dorsal columns
Senses Pain, temperature, touch, vibration and proprioception
Destination: somatosensory cortex

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43
Q

Use of the ventral-postero medial nucleus?

A

Trigeminal and gustatory pathways
Responsible for face sensation and taste
Destination: primary somatosensory cortex

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44
Q

Lateral geniculate nucleus?

A

CN 2
Responsible for vision
Destination: Calcarine sulcus
Lateral=light

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45
Q

Medial geniculate nucleus?

A

Input: superior oliver and inferior colliculusof tectum
Senses:

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46
Q

Ventral lateral nucleus?

A

Input: basal ganglia, cerebellum
Senses: Motor
Destination: Motor Cortex

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47
Q

What is the limbic system?

A

Collection of neural structures involved in emotion, long-term memory, olfaction, and behavior modification

Structures include: hippocampus, amygdala, fornix, mammilary bodies, cingulate gyrus

(responsible for feeding, fleeing, fighting, sex)

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48
Q

What happens when the following dopaminergic pathways are damaged?

Mesocortical
Mesolimbic
Nigrostrial
Tuberoiunfundibular

A

Mesocortical: negative symptoms (flat affect and limited speech, antipsychotic durgs have limited effect)

Mesolimbic: positive symptoms (delusions, hallucinations),primary target of anti-psychotics

Nigrostriatal: decreased activity leads to extrapyramidal symptoms such as dystonia, akathisia, parkinson, tardive dyskinesia

Major Dopinergic pathway in the brain, significantly affected by movement disorders and antipsychoti drugs

Tuberinfundibular: decreased in activity leads to increase in prolactin, galactorreha and gynecomastia

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49
Q

Function of the cerebellum?

A

Modulates movement and aids in coordination and balace

Input: contralateral cortex via middle cerebeller peduncle

ipsilateral cerebellar pununcle from the spinal cord

Output: sends information to the contralateral cortex, via the superior cerebellear peduncle

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50
Q

Lateral lesions of the cerebellum?

A

Voluntary movement of extremitires with propensity to fall toward the injured, ipsilateral side

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51
Q

Medial leisions?x3

A

Involvement of the mideline structures (vermal cortex, fastigial nuclei)

will have truncal ataxia, nystagmus, head tilting, and affect axial and proximal gait.

Will generally have bilateral motor deficits affecting axial and proximal limb musuclature

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52
Q

Functions of Basal Ganglia?

A

Recieves cortical input (provides negative feedback to cortex to modulate movement)

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53
Q

What does striatum affect?

A

putamen (motor) + caudate (cognitive)

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54
Q

What does lentiform affect?

A

Putamen + globus pallidus

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55
Q

Movement disorders: athetosis?

A

Slow, writhing movements of the fingers

Lesion within the Basal gangla (huntingtons)

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56
Q

Movement disorders: Chorea?

A

Sudden, jerky, purposeless movement

Basal ganglia lesion

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57
Q

Essential tremor?

A

High frequency tremor with sustained posture (outstrected arms) worsened with movements or when anxious

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58
Q

Hemiballismus?

A

Sudden, wild flailing of 1 arm, +/- ipsilateral leg

Usually due to contralateral subthalamic nucleus

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59
Q

Intention tremor?

A

slow, zigzagging motion when pointing/extending toward a target

Due to cerebellar dysfunction

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60
Q

What is myoclonus?

A

sudden, brief, uncontrolled muscle contraction

Will have jerks, hiccups, common abnormalities in the renal and liver failure

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61
Q

What is a resting tremor?

A

Uncontrolled movement of the distal appendages
Tremor is allreviated by intentional movement
Occurs as a pill-rolling tremor (Parkinsons)

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62
Q

Characteristics of parkinson’s disease?

A

Degenerative disorder for the CNS associated with Lewy bodies
Loss of dopaminergic neurons

Tremor
Rigidity
Akinesia
Postural instability
Shuffling gait
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63
Q

Characteristics of Huntington’s disease?

A 
Autosomal dominent 
Symptoms manfest between 20-50 years of afe
Chloriform movemebts
agression
Depression 
Dementia
Increase dopamine
Decrease dopamine
Decrease GABA
Decrease Ach
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64
Q

What is aphasia?

A

Inability to understand, speak, read and write

higher learning language deficit

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65
Q

Dysarthria?

A

Motor inability to speak (movement deficit)

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66
Q

Broca aphasia?

A

Non fluent speech
Comprehension is intact
Reptition is impaired
Due to inferior frontal gyrus of frontal lobe

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67
Q

Wernicke’s aphasia?

A

Speech fluidity: fluent
Comprehension: impaired
Repitition: impaired
Wernicke is wordy but makes no sense

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68
Q

Conduction aphasia?

A

Fluidity: fluent
Comprehension: intact
Repeatition Impaired

Caused by damage to the arcuate fasciculus

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69
Q

Global aphasia?

A

Fluidity: non
Comprehnesion: impaired
Repitition: impaired
Region: arcuate fasciculus (Broca and Wernicke’s areas are affected)

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70
Q

Transcortical motor aphasia?

A

Fluidity: nonfluent
Comprehension:intact
Repetition : Intact
Affects the frontal lobe around Broca (but Broca area is spared)

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71
Q

Transcortical sensory apahsia?

A

Fluidity: fluent
Comprehension: impaired
Repitition: Intact
Affects the temporal lobe around the wenicke area, but the wernicke is spared

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72
Q

Transcortical mixed

A

Broca and Wernicke area and arcuate fasciculus remain intact, but surrounding watershed areas are affected

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73
Q

Leisions of the brain associated with amygdala?

A

Kluver-Bucy syndrome (uninhibited behavior: hyperphagia, hypersexuality, hyperorality)

Associated with HSV-1 encephalitis

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74
Q

Lesions to the frontal lobe?

A

Disinhibition and deficits in concentration

Re-emergence of primitive reflexes

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75
Q

Leisions of nondominent parietal cortex?

A

Hemispatial neglect syndrome (agnosia of contralateral side of the world)

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76
Q

Lesions of the dominenet parietal cortex?

A

Agraphia, acalculia, finger agnosia, left-right disorientation

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77
Q

Lesions of reticular activating system (midbrain)

A

Reduced levels of arousal and wakefulness

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78
Q

Mamillarybody lesions?

A

Wernicke Korosakoff syndrome
Confusion
Ophtalmopelgia, ataxia, memory loss, anterograde and retrograde amnesia
Confabulation, personality changes

Associated with thiamine (B1 deficiency) due to ETOH

Can be associated with ataxia, nystagmus, and confusion

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79
Q

Lesions of the of the basal ganglia?

A

Tremor at rest
Chorea
Athetosis

Parkinsons Disease
Huntington’s disease

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80
Q

Lesions of the Cerebeller hemisphere?

A 
Limb tremore
limn atazia 
lose of balance
Ipsilateral deficits 
Fall toward side of the lesions

Associated with chronic ETOH use

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81
Q

Lesions of the cerebellar vermis?

A

Truncal ataxia
Dysarthria
Vermis is centrally located

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82
Q

Lesions of the subthalamic nucleus?

A

Contralateral hemiballismus

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83
Q

Lesions of the hippocampus (bilateral)

A

Antegrade amnesia (inability to make new memories)

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84
Q

Paramedian pontine reticular formation leisions?

A

Eyes that look away from the side of the leision

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85
Q

Frontal eye field leisions?

A

Eyes look toward the leisions

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86
Q

How does cerebral brain perfusion occur?

A

Relies on autoregulation (driven by PCO2)

When there is severe hypoxia then (PO2 will modulate perfusion)

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87
Q

what does cerebral perfusion rely upon?

A

The gradient between the mean arterial pressure (MAP)and the ICP

Decrease in BP or increase in ICP leads to decrease cerebral perfusion pressure

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88
Q

What is therapeutic hyperventilation?

A 
Decrease PCO2:
leads to vasoconstriction
decrease cerebral blood flow
Decrease in ICP
Used to treat acute cerebral edema (due to stroke)
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89
Q

What is the CPP calculation?

A

CPP= MAP-ICP

If the CPP is zero, there is no cerebral perfusion, leading to brain death

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90
Q

What is area of distribution for anterior cerebral artery?

A

Anteromedial surface

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91
Q

Area of distribution of middle cerebral artery?

A

Lateral surface of the brain

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92
Q

Area supplied by the posterior cerebral artery?

A

Posterior and inferior surfaces

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93
Q

What are the watershed areas?

A

Areas between the anterior and middle
Between the posterior and middle cerebral arteries
Damage due to severe hypotension (upper leg/upper arm weakness) defects in higher order visual processing

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94
Q

what is the circle of Willis?

A

Anterior cerebral artery, connects to middle cerebral artery to the posterior cerebral artery, to the internal carotids

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95
Q

Stroke in the middle cerebral artery?

A

Motor and sensory cortices (upper limb and face)
Temporal lobe: Wernicke’s area
Frontal lobe (Broca)

Symptoms: contralateral paralysis and sensory loss of the face and upper limb

Aphasia if in the dominenet left hemisphere

Hemineglect if lesion affect non dominant side

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96
Q

Lesion of the anterior cerebral artery?

A

Motor and sensory lower limb

Contralateral paralysis and sensory loss (lower limb)

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97
Q

Lenticulostriate artery?

A

Striatum and internal capsule
Leads to contralateral paralysis and sensory loss
(face and body(

Will have absence of cortical signs including : neglect, aphasia, visual field loss

This is a common location of the lacunar infarcts, secondary to unmanaged hypertension

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98
Q

Lesions of the anterior spinal artery?

A 
Contralateral paralysis (upper and lower limbs) 
Decreased contralateral proprioception 
Ipsilateral hypoglossal dysfunction (tongue deviates ipsilaterally)
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99
Q

Medial medullary syndrome?

A

Caused by infarct of the paramedian branches of Anterior spinal artery or the vertebral arteries.

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100
Q

Lesions of the posterior inferior cerebral artery

A 
will affect:
Lateral medulla
Lateral spinothalamic tract 
Spinal trigeminal nucleus 
Sympathetic fibers 
Inferior cerebral penduncle
Symptoms: 
Vomiting
Vertigo 
Nystagmus 
Decrease in pain and temperature sensation from ipsilateral face and contralateral body
Dysphagia 
Hoarseness
Decrease in gag reflex 
Ipsilateral Horner syndrome
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101
Q

What is the laterl medullary (Wallenberg syndrome)?

A

Nucleus ambiguous effects are specific to posterior inferior cerebellar artery

“Don’t pick a horse (hoarseness) that can’t eat (dysphagia)

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102
Q

Lesions of the anterior, inferior cerebellar artery?

A

Lateral pons (cranial nerve nuclei, vestibular nuclei, facial nucleus, spinal trigeminal nucleus, cochlear nuclei)

Spinothalamic tract
Corticalspinal tract
Sympathetic fibers

Middle and inferior cerebellar peduncles

Symptoms:
Vomiting
Vertigo
Nystagmus 
Paralysis of the face
Decrease lacrimation
Decrease salivation
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103
Q

Lesions of the basal artery?

A

Pons
Medulla
Lower midbrain
Corticospinal, corticobulbar tracts (ocular cranial nerve nuclei)

Preserved consciousness
Vertical eye movement
Lost off voluntary facial, mouth, and tongue movements
Loced in syndrome

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104
Q

Lesions in the posterior cerebral artery?

A

Area of leision: occipital cortex and visual cortex

Leads to contralateral hemianopia with macular sparing

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105
Q

Lesions of the middle cerebral artery?

A

Rupture may cause ischemia in the MCA distribution (contralateral upper extremity, facial hemiparesis and sensory deficits)

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106
Q

Central post stroke pain syndrome?

A

Neuropathic pain due to thalamic lesions
Initial parestheisis followed in weeks to months by allodynia and dysesthesia

Occurs in 10% of stroke patients

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107
Q

Epidural hematoma?

A

Rupture of middle meningeal artery (branch of maxillary artery) usually due to skull fracture

Lucid interval followed by rapur expansion under systemic arterial pressure

Can cause transtentoria herniation

CN III palsy

CT will show biconvex (lentiform) hyperdense blood collection that doesn’t

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108
Q

Subdural hematoma?

A

Rupture of the bridging viens
Can be acute, will have traumatic, high energy impact or chronic due to to mild trauma, cerebral atrophy, elderly , ETOH

Seen in shaking babies

Predisposing factors: brain atrophy and trauma

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109
Q

Subarachnoid hemorrhage?

A

Rupture of aneurysm (such as saccular aneurysm) or AV malfomation

Rapid time course
Starts with the worst headache of their lives
Will have a bloody or yellow spinal tap
Can occur with ischemic infarct

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110
Q

How to prevent transformation of subarachnoid hemorrhage from an ischemic stroke?

A

Give nimodipine

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111
Q

What is intraparenchymal hemohage?

A

Commonly caused by systemic hypertension
Also seen with amyloid angiopathy
Vasculitis or neoplasm

May be secondary to reperfusion injury within ischemic stroke

Typically occurs in basal ganglia and internal capsule
(Charcot-Bouchard aneurysm of the lenticulostriate vessels

Can be lobar

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112
Q

When does irreversible damage to the brain occur?

A

After 5 minutes of hypoxia

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113
Q

What are regions most vulnerable for damage in the brain?

A

Hippocampus
Neocrotex
Cerebellum
Watershed areas

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114
Q

What type of test is required for a stroke?

A

Non contrast CT to exclude hemorrhage (before tPA can be given)

CT detects ischemic changes 6-24 hours after

MRI can detect ischemia within 2-30 minutes

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115
Q

What are the three types of ischemic stroke?

A

Thrombotic :due to clot formation directlyat the site o infarction (commonly MCA) over atherosclerotic plaque

Embolic : embolus from other part ofthe body, obstructs the vessel (Can affect multiple vascular territories)

For example: afib, DVT or presence of PFO

Hypoxic: due to hypoperfusion or hypoxemia
(Common during cardiovascular surgery) tends to affect watershed areas

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116
Q

When can TPA be used for stroke?

A

If within 3-4.5 hours of onset

No risk of hemorrage

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117
Q

How to reduce the risk of stroke?

A 
ASA and Plavix 
Optimum control of blood pressure 
Control blood sugar
Control lipids
Treat A fib
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118
Q

Definition of TIA?

A

Brief, reversible episode of neuro dysfunction without acute infarct (MRI -) usually resolves within 15 minutes

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119
Q

What are dual venous sinuses?

A

Large venous channels that run through the dura

Drain blood from cerebral veins and recieve CSF from arachnoid granulations

Empty into the internal jugular vein

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120
Q

What is a venous sinus thrombosis?

A

Presents with signs/symptoms of increase ICP

Headache, seizure, focal neurological deficits.

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121
Q

what conditions are associated with Venous sinus thrombosis?

A

Hypercoagulable states (pregnancy, OCP, factor V Leiden)

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122
Q

Idiopathic intracranial HTN?
Symptoms?
Risk?

A

Increase in ICP with no cause on imaging ( no hydrocephalus, or obstruction of CSF flow)

Symptoms: headache, diplopia (CN V1 palsy)
No change in mental status
Papilloedema
Lumber puncture has increased opening pressure and provides headache relief

Treatement: weight loss, acetazolamide, topimarate, invasive procedures for refractory cases

(repeat lumber puncture
CSF shunt placement
Optic nerve fenestration

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123
Q

What does hydrocephalus mean?

A

Increase in CSF volume with ventricular dilation and increase in ICP

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124
Q

What is communicating hydrocephalus>

A

Decrease CSF asbsorption by arachnoid granulations

Increase in ICP leading to pailledema and herniation

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125
Q

What is normal pressure hydrocephalus?

A 
Elderly
Idiopathic 
CSF pressure only periodically elevated 
Expansion of the ventricles 
Distorts fibers of the corona radiata
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126
Q

What are the triad of normal presssure hydrocephalus?

A

Urinary incontinence
Ataxia
Cognitive dysfunction

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127
Q

What is the cause of non communicating (obstructive hydrocephalus)

A

Caused by structural blockage of CSF circulation within the ventricular syste

Usually caused by stenosis of aqueduct of Sylvius
Colloid cyst blocking foraman of Monroe
Tumors

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128
Q

What are conditions of hydrocephalus mimics?

A

Increase appearance on CSF imaging, but actually due to decreased brain tissue

Causes neuronal atrophy
(Alzheimer disease, advanced HIV, Pick disease)

ICP is normal
Triad is not seen

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129
Q

How mant spinal nerves are there?

A

There are 31 pairs of spinal nerves

8 cervical 
12 thoracic
5 lumbar
5 saccral 
1 coccygeal
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130
Q

Where do the spinal nerves exit?

A

C1-C7 above the corresponding vertebraw

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131
Q

Where does the subarachnoid space extend to?

A

The lower border of the S2 vetebrae

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132
Q

Where do lumber puncture usually performed?

A

L3 and L4
or
L4 and L5

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133
Q

Describe the anatomy of the spinal cord?

A 
white matter on the outside
Grey matter is butterfly on the inside
CSF directly in the middle 
Venticle fissue 
Dorsal median sulcus
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134
Q

what are the parts of the dorsal column?

A

Gracile

Cuneate

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135
Q

What is the dorsal column responsible for?

A

Proprioception

Fine touch

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136
Q

Briefly describe the Dorsal Column Tract?

A

Responsible for: fine touch and proprioception
There are 3 axon bodies

Sensory and nerve endings in dorsal root ganglion—> entrs the spinal cord—> ascends ipsilaterally and synapses in the cuneatus or gracilus medulla —> decussates in medulla (at this point contralaterally) —> synapses in the thalamus

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137
Q

Briefly describe the spinothalamic tract?

A

Responsible for : Pain, temperature (anterior for crude touch and pressure)

Sensory nerve ending —> to the dorsal root ganglions–> enters the spinal cord—>ipsilateral in the spinal cord—> decussates in the anterior white commisure—-> ascends contralaterally —> ends in the sensory cortex

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138
Q

Briefly describe the lateral corticospinal tract?

A

Responsible for: Voluntary movement of the contralateal limbs

Upper motor neuron: descends ipsilaterally (through internal capsule) —> decussade at the caudal medulla—> descends contralaterally—> cell body in the anterior horn—> lower body neuron leaves the spinal cord

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139
Q

What are characteristice of lower moter neuron leision vs upper motor neuron?

A 
Lower Motor Neuron:
Atrophy
Fasciulations Flaccid paralysis 
Decrease of reflexes 
Decrease of Tone 
Signs of Upper Motor Neuron Leison:
Increase reflexes 
Increase tone
Babinsky _ 
Spastic paralysis + 
Clasp knife spascitiy
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140
Q

Characteristics of Poliomyelitis and Werdnig-Hoffmann disease?

A

Congential degeneration of the anterior horn of spinal cord

Usually have lower motor neuron leisions
Floppy baby
Have hypotonia and tongue fascilations
Usually death at 7 months

Difference between Poliomyelitis and Werdning Hoffmann- symmetric weakness

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141
Q

Characteristics of amyotrophic lateral sclerosis?

A

Combined upper and lower motor deficits wih no sensory/bowel/bladder defects

(loss of cortical and spinal cord neurons respectively)
Have assymetric weakness, with fascilations and eventual atrophy

Known as Lou Gehrig’s disease

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142
Q

Characteristics of complete occulsion of the anterior spinal artery?

A

Spares dorsal column

Anterior spinal artery is a watershed area.

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143
Q

Charactersitics of Tabes dorsalis?

A

Caused by 3 syphilis

Degeneration or demyelination of dorsal columns and roots leading to ataxia and poor coordination

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144
Q

Characteristics of Syringomyelia?

A

Syrinx can expand and damage anterior commisure of spinothalamic tract

Bilateral loss of pain and temperature sensation in cape-like distribution

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145
Q

Characteristics of Vitamin B deficiency?

A

Sub acute degeneration (demyelination of Spinocerebeller tracts), lateral corticospinal tracts, and dorsal column.

Leads to ataxia, paresthesia, impaired position/vibration

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146
Q

What is poliomyelitis?

A

Caused by poliovirus (fecal-oral transmission)
Replicates in the oropharynx and small intestine before spreading via bloodstream to the CNS
Infection causes destruction of the cells in anterior horn of the spinal cord (LMN death)
Signs of polio: weakness, hypotonia, flaccid paralysis, fasciculatios, hyporeflexia, muscle atropy

Signs of infection: malaise, headache, fever, nausea

CSF shows: increased WBC with increase in protein

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147
Q

What is Friedereich’s ataxia?

A

Autosomal recessive trinuclotide repeat (GAA) on chromosome 9

Impingement in mitochrondiral functioning

Degeneration of multiple spinal chord tracts

Muscle weakness and loss of DTR (vibratory sense, proproception, staggerring gait, frequent failing, nystagmus. dysarthrai, hammer toes, diabetetes, hypertrophic cardiomyopathy

In childhood presents with kyphoscoliosis

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148
Q

What is Brown-Sequard syndrome?

A

Hemisection of the spinal chord

Ipsilateral UMN signs below the level of the leision (due to corticospinal tract damage)

Ipsilateral loss of tacitile vibration, proprioception sense below the level of the leision due to dorsal column damage

Contralateral pain and temperature loss below the level of the leision (due to spinothalamic tract damage)

Ipsilateral loss of all sensations at level of the leision

Ipsilateral LMN signs (flaccid paralysis) at the level of leision

If leision occurs above the T1, patient may present with ipsilateral Horner syndrome due to damage of the oculosympathetic pathway

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149
Q

dermatome C2?

A

Posterior half of the skull cap

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150
Q

dermatome of C3?

A

High turtleneck shirt

151
Q

dermatome of C4?

A

Low coller shirt

152
Q

dermatme of C6?

A

arm and includes the thumbs

153
Q

T4?

A

at the nipple

154
Q

T7?

A

at the xiphoid process

155
Q

T10?

A

at the umbolicus

156
Q

L1?

A

At the inguinal ligametn

157
Q

L4?

A

Includes the kneecaps

158
Q

S2, S3, S4?

A

erection and sensation of penile and anal zones

159
Q

Where does diaphgram and gallbladder pain refer?

A

Referred pain to the shoulder via the phrenic nerve

160
Q

reflexes of the biceps?

A

C5 nerve root

161
Q

Reflexes of the triceps?

A

C7

162
Q

Reflexes of the patallea?

A

L4

163
Q

Reflexes of the achilles?

A

S1 nerve root

164
Q

when do primitive reflexes occur?

A

Inhibited by mature developing frontal lobe
Can reemerge if the adult has frontal lobe leisions
Leads to loss of inhibition of the reflexes

165
Q

Moro reflex?

A

Hang on for life

Abduct and extend arms when startled (and then draw together)

166
Q

Rooting reflex?

A

Movement of the head toward one side if cheek or mouth is stroked

167
Q

Sucking reflex?

A

Sucking response when roof of the mouth is touched

168
Q

Palmar reflex?

A

Curling fingers if palm is stroked

169
Q

Plantar reflex?

A

Dorsiflexion of large toe and fanning of other toes with plantar stimulation

Babinski sign: presence of this reflex in an adult (UMN)

170
Q

Galant reflex?

A

Stroking along one side of the spine while newborn is in ventral suspension (face down) causes lateral flexion of the lower body toward simulated side

171
Q

Which cranial nerves are above the pons?

A

I
II
III
IV

172
Q

Cranial nerves in the pons?

A

V
V1
V11
V111

173
Q

Cranial nuclei that are medial?

A

III
IV
VI
X11

174
Q

function of the pineal gland?

A

Melatonin secretion

Circadian rhythms

175
Q

Superior colliculi?

A

Conjugate vertical gaze center

note, your eyes are above your ears, and the superior colliculus are above the inferior colliculus..ears

176
Q

Inferior colliculi?

A

Auditory

177
Q

Parinaud syndrome?

A

Paralysis of conjugate vertical gaze due to leision of superior colliculli (stroke, hydrocephalus

178
Q

Cranial nerve I?

A

Olfactory

179
Q

Cranial nerve II

A

Optic

180
Q

Cranial nerve III

A

Oculomotor (eye movement), pupillary constriction, accomodation

181
Q

Cranial nerve IV?

A

Trochlear

eye movement

182
Q

Cranial nerve V?

A

Trigeminal

Mastication, facial sensation (opthalmic, maxillart, mandibular, diviison) somatosensation of anterior 2/3 of the tongue

183
Q

Cranial nerve VI

A

Abducens (eye movement)

184
Q

Cranial nerve VII

A 
Facial movement
Taste from anterior of the 2/3 of the tongue 
lacrimation
salivation
eyelide closing 
Auditory volume
185
Q

Vestibulocochlear VIII?

A

Hearing and balance

186
Q

Glossopharyngeal IX?

A

Taste and sensation from posterior 1/3 tongue, swallowing, salivation (parotid gland)
Monitoriing carotid body, sinus, chemo and baroreceptors

187
Q

Vagus X?

A

Taste from supraglottic region
Swallowing
Soft palate elevation
talking, coughin, parasympathetics to thoracoabdominal viscera

188
Q

Accessory XI

A

Head turning, shoulder shrugging, SCM, trapezius

189
Q

Hypoglossal XII

A

Tongue movement

190
Q

What are the vagal nuclei nucleus solitarius?

A

Responsible for visceral sensory information
(taste, baroreceptors, gut distention)

Cranial nerve VII, IX, X

191
Q

Nuclue ambigous?

A

Motor innervation of the pharynx, larynx, upper esophagus

IX, X, XI

192
Q

Dorsal motor nucleus?

A

Sends autonomic parasympathetic fibers to the heart,lung, and upper GI

193
Q

Corneal nerve reflex?

A

Afferent: V1 opthalmic
Efferent:V2 (temporal branch)

194
Q

Lacrimation reflex?

A 
Afferent V1 (loss of V1 does not preculude emotional tears) 
Efferent: V11
195
Q

Jaw jerk reflex?

A

Afferent: V3 (sensory-muscle spindle from masseter)
Efferent: motor-masseter

196
Q

Pupillary reflex?

A

Afferent II

efferent: III

197
Q

Gag reflex?

A

Afferent IX

Efferent X

198
Q

CN 5 lesion?

A

Jaw deviates toward the side of the leision due to unopposed force from the opposite ptergoid muscle

199
Q

CN X lesion?

A

Uvula deviates awat from the side of the leision (weak side collapses_

200
Q

CN X1 lesion?

A

weakness turning head to contralateral side of the leision (SCM)) shoulder droop on side of lesion (trapezius)

201
Q

CN XII leision?

A

LMN leision (tongue deviates toward the side of the leision) lick your wounds

202
Q

What are the mastication muscles?

A

Masseter
Temorarlis
Medial pterygoid

203
Q

Facial nerve leision (upper motor neuron)

A

Destruction of motor cortex or connection between motor cortex and facial nucleus in the pons

Contralateral paralysis of lower muscles of facial expression

Forehead is spared due to bilateral UMN innervation

204
Q

Lower motor neuron leision?

A

Destruction of facial nuclues or CN VII anywhere along it’s course
Ipsilateral paralysis of upper and lower muscles (facial exoression)

hyperacusis (loss of taste and sensation to the anterior tongue)

205
Q

Clinical syndrome of CN VII leision?

A

Causes partial or complete loss of function depending on location or severity of the leision

Can cause partial or complete loss of function

206
Q

What is Bell’s palsy?

A

Caused by Lyme diseas, herpes, herpes zoster, sarcoidosis trauma, DM

207
Q

What is treatment of Bell’s palsy?

A

Corticosteroids
Acyclovir
Most have gradual return of function

208
Q

What are cavernous sinus?

What is cavernous sinus syndrome?

A

Collection of sinus on either side of the pituitary gland
Blood from eye and superficial cortex lead to the cavernous sinus, to the internal jugular vien

Cavernous sinus syndrome: variable ophtalmoplegia, decreased corneal sensation, Horner syndrome, decreased maxillary sensation

Can be caused by pituitary mass effect
Sinus thrombosis (due to infection)
209
Q

What is the outer ear?

A

visible portion (pinna) includes
auditory canal
eardrum
Transfers waves via vibration of the eardrum

210
Q

What is the middle ear?

A

Air filled space with three bones, ossicles, malleus, incus, stapes

Ossicles conduct and ampligy sound from eardrum to inner ear

211
Q

what is the inner ear?

A

Snail shaped, fluid filled cochlea
Have basilar membrane that vibrates 2 to sound waves
Vibration is transduced via special hair cells —> auditory nerve signalling to the brain stem

212
Q

Where is low frequency heard?

A

Apex near the helicotrema

213
Q

Where is high frequency heard?

A

At the base of cochlea

214
Q

What is conducive hearing loss?

A

Rinne test abnormal (put a tuning fork on mastoid), the air should be better then the bone (512 HZ)
(bone more then air)

Webber test: localized to affected ear (on forehead) and both ears should hear the same

215
Q

What is sensorineural hearing loss?

A 
Rhine test (air more then bone)  NORMAL
Weber test (localized to the affected ear)
216
Q

What is noise induced hearing loss?

A

Damage to sterociliated cells in organ of Corti
Loss of high frequency hearing lost first
Sudden extremely loud nosed can result in hearing loss due to tympanic membrane rupture

217
Q

Cholestetoma?

A

Overgrowth of desquamated keratin debris within the middle ear

This can lead to conductive hearing loss

218
Q

What is the pathway of aqueous humor?

A

Produced by non pigemneted epithelium of the ciliary body

Travels over the trabecular meshwork, through canal of
Schlemm (90%)

10% goes through the uveoscleral outflow

219
Q

How to decrease aqueous humor?

A

Decrease production by B-blockers, alpha agonsits and carbonic anhydrase inhibitors
alpha agonists

Can also work on the uveoscleral outflow:
Drainage into the uvea and sclera (increase prostaglandin agonsit

220
Q

Hyperopia?

A

eye too short for refractive power of cornea and lens

(light focused behind the retina

221
Q

Myopia?

A

eye too long for refractive power of the cornea and lens (focused in front of the retina)

222
Q

Astigmatism?i

A

abnormal curvature of the cornea, with refactive power at different axis

223
Q

Presbyopia?

A

Age related impaired accomadation (diffculty focusing on near objects due to decreased lens elasticity

224
Q

Characteristics of cataract?

A

Painless, bilateral opacification of the lens
Results in decrease of vision
Increased with age, smoking, ETOH, sunlight exposure
DM
Trauma
Infection

225
Q

What are congential causes of catacts?

A 
TORCH (rubella) 
Marfan sundrome
Alport Syndrome
Myoptonic dystrophy
Neurofibromatosis 2
226
Q

What is glaucoma? What are the treatment?

A

Optic disc atrophy with charactersitic thinning of the outer rim of optic nerve

Usually due to elevated intra-ocular pressire and progressive loss of periphereal vision

227
Q

Open angle glaucoma?

A

Increase with age
Increase with African American race
Family history
More common in US

228
Q

what are secondary causes of glaucoma?

A

Blocked trabecular meshwork from WBC (uvetis)
RBC (vitroud hemorrage)
Retinal detachement

229
Q

What is closed angle glaucoma?

A

Enlargement or movemebt of the lens agains the central iris
Obstuction of the normal aqeous flow through the pupil
Fluid builds up behind the iris (pushing periphereal iris against the cornea) and impedes flow through the trabecular network

230
Q

What are secondary causes of closer or narrow angle glaucoma?

A

Hypoxia from retinal disease (DM, vein occlusion)

Induces vasoproliferation in iris, that contracts angle

231
Q

What is chronic vs Acute angle glaucoma?

A

Chronic: often assymptomatic with damage to the optic nerve and periphereal vision

Acute closure: opthalmic emergenvy, the IOP pushes the iris foreward—> angle closes abruptly
Very painful, red eye, sudden vision loss, halos around lights

Rock hard eye
Frontal headache

DO NOT give epinephrine because of the mydraitic effect

232
Q

Characterstics of conjunctivitis?

A

Inflammation of the conjunctiva (red eye)
Allergic: itchy, bilateral
Bacterial: pus, treat with antibiotics
Viral: most common (usually adenovirus) mucos discharge with swollen preauricular node. Usually self resolving

233
Q

What is uveitis?

A

Inflammation of the uvea

names are specific to the location within the affected eye

234
Q

What are the different areas?

A 
Anterior uveitits 
Intermediate uveitisi 
Pars planitis
Posterior uveitis 
Chorioditis or retinitis
235
Q

What is a hypopyon?

A

Accumulation of pus within the anterior chamber
Conjunctoval redness
Associated with systemic inflammatory disoders (sarcoidosis, rheumatoid arthritis, juvenile idopathic arthritis, HLA-B27 associated conditions

236
Q

Characteristics of age-related macular degeneration?

A

Degeneration of the macula (central area of retina)

Causes distortion and eventul loss of vision

237
Q

What is dry macular degeneration?

A

Dry: nonexudative > 80% depositions of yellow extracellular material in and between Bruch membrane and retinal pigment

238
Q

what is wet macular degeneration?

A

Rapid loss of vision due to bleeding 2nd to choroidal neovascularization

Treat with anti-VEGF (injections, ranibizumab)

239
Q

What is diabetic retinopathy?

A

Neoproliferative (damaged capillaries, leak blood)
Lipids and fluids seep into the retina
Can lead to hemorrages.

240
Q

What is retinal vein occlusion?

A

Blockage of central or branch retinal vein due to compression from nearby arterial atherosclerosis

Leads to retinal hemorrhage and venous engorgement and edema

241
Q

What is retinal detachement?

A

Seperation of neurosensory layer of the retina (photorecepter layer with rods and cones from outermost pigmented epithlium) normally shields light

Leads to degeneration of photorecpetors and leads to vision loss.

242
Q

What causes retinal detachement?

A

Retinal breaks
Diabetic traction
Inflammatory effusions
Visualized on fundoscopy

243
Q

Breaks are more common in which ?

A

Patients with high myopia or history of head trauma
Usually oreceded by posterior vitrous detachment (flashes or floaters) and eventual loss of vision (like a curtain drawn down).

244
Q

What is central artery occlusion?

A

Acute, painless, monocular vision loss
The retina is cloudy with attenuated vessels and cherry red fovea
Evaluate for embolic sources.
(carotid artery atheroscleoris, cardiac vegetation, PFO)

245
Q

What is Retinitis pigmentosa?

A

Inherited retinal degeneration
Painless, progressive vision loss, starting with night blindness

Bone spicule shaped deposit arund macula

246
Q

What is retinitis?

A

Retinal edema and necrosis (leading to scar)
Often viral *CMV, HSV, VSV)

Can be bacterial or parasitic

247
Q

what is papilledema?

A

Optic disc swelling (usually bilateral) due to increased ICP

Enlarged blind spot and elevated optic disc with blurred margins

248
Q

What is responsible for pupillary control?

A

Miosis
Constriction is parasympatetic
1st neuon is Edinger-Westphal nucleus to ciliary ganglion via CN III

2nd neuron: short ciliary nerves to pupillary sphincter muscle

249
Q

what is the pupillary light reflex?

A

Light enters the reinta
Sends a signal via CN II
Enters the brain and activates bilateral Edinger-Westphal nuclei
Pupils contract bilateral

(Illumination of 1 eye, results in bilateral pupillary constriction)

250
Q

What is responsible for mydriasis?

A

dilatation (sympathetic)
1st neuron: hypothalamus to ciliospinal center C8-T2
2nd neuron: exit T1 to superior cervical ganglion
3rd neuronL plexus along the internal carotid
(through cavernous sinus, and enters the orbit)

251
Q

What is a Marcus Gunn Pupil?

A

afferent nerve defect (due to optic nerve damage or severe retinal injury)

Decrease in bilateral pupillary constriction when light is shone to the affected eye.

Tested with the swinging flashlight test

252
Q

What is Horner’s syndrome?

A

1) Sympathetic denervation of the face
a) Ptosis : slight drooping of the eyelid (superior tarsal muscle)
b) Anhidrosis (absence of swearing) and flushing on affected side of the face
c) Miosis (pupil constrcition)

253
Q

What are the conditions associated with the Horner syndrome?

A

Pancoast tumore
Brown- Sequrd syndrome
Late stage syringmyelia

254
Q

What are the muscles of the eye?

A 
Superior rectus muscle
Lateral rectus muscle 
Inferior oblique muscle (inferior rectus muscle) 
Medial rectus muscle 
Trochlea
Superior oblique muscle
255
Q

What is the formula to remember what nerves innervate which muscle?

A

LR6 SO4 R3
Lateral rectus CN 6
Superior Oblique CN 4
Rest: CN 3

256
Q

What affects CN 3 (motor and parasympathetic output)?

A

Motor: affected by vascular disease (DM, soribital)
Due to decrease diffusion of O2 and nutrients
Leads to ptosis

Parasympathetic: fibers on the periphery are first affected by compression.

Posterior communicating artery aneurysm
Uncal herniation
Will have diminsihed or absent pupillary reflex
Blown pupil or down and out gaze

257
Q

What is CN IV damage?

A

Eye move upward, particularly with contralateral gaze

And head tilt toward the side of the leision

258
Q

CNVI damage?

A

Medially directed eye that cannot abduct

259
Q

Lesion causing bitemporal anopia?

A

Pituitaty lesion (chiasm)

Defect normal normal \defect

(Leasions on outside of both eyes)

260
Q

Left homonymous hemaniopia?

A

defect - normal defect-normal

261
Q

left upper quadrant anopia?

A

1/4 of both upper eyes (facing to the left)

Right temporal lesion MCA

262
Q

Left lower quadrant anopia?

A

Right parital lesion, MCA

263
Q

Left hemainopia with with macular sparing>

A

PCA infarct

264
Q

Central Scotoma?

A

Macular Degeneration

265
Q

what is internuclear ophtalmoplegia?

A

Lesion in the medial longitudinal fasiculus (pair of tracts that allow crosstalk between CN V1 and CN 3

The MLF coordinates both eyes to move in the same horizontal direction

Highly myelinated (must communicate quickly)

Leisions can be unilateral or bilateral

Usually seen in multiple sclerosis

Will have one eye that has imparied adduction, while the other one has nystagmus

266
Q

What are characteristics of Alzeihmers?

A

Associated with Apo E2 (decrease in risk of the sporadid form)

Apo E4: increase the risk of the sporodic form

APP presenilin-1 and presenilian-2 (famililal forms 10%) with earlier onset.

267
Q

What are histological findings of Alzehiemers?

A 
Widespread cortical atrophy 
Decrease in ach 
Senile plaques in the grey matter 
Intracranial hemorrhage (Amyloid B) 
Neurofibrillary tangles
268
Q

Characteristics of early fronto-temoporal dementia?

A

Early changes in personality and behavior
Can have progressive aphasia
May have associated disorders like parkinsonian, ALS like (UMN/LMN) degeneration

269
Q

What is Lewy body dementia?

A

Dementia with visual hallucinations

Has parkinson features

270
Q

Vascualar dementia?

A

Due to multiple arterial infarcts
Step wise decline in cognitive dysfunction
Second most common demntia in the elderly

271
Q

Creutzfeldt-Jakob disease?

A

Rapidly progressing demntia
Has startle myoclonus
Has spongiform cortex
Presence of prions

272
Q

What are other causes of dementia?

A 
Syphilis
HIV
hypothyroidism 
B3 and B12 deficiency 
Wilson's disease 
Hydrocephalus
273
Q

What is osmotic demylination?

Causes?

A 
Acute paralysis 
Dysarthria 
Dysphagia 
Diplopia 
Loss of consciousness
Massive axonal demylination 
What are causes of demylination? 
Usally iatrogenic (caused by overly rapid correction of hyponatremia)

Overly quickly correcting hypernatremia too quickly lead to cerebral edema

274
Q

What is multiple scleorosis?

A

Autoimmune and demyelination of CNS (brain and spinal cord)

Can present with optic neuritis (sudden loss of vision resulting in Marcus Gunn pupils)

Usually affects women in their 20s and 30s

275
Q

What is the Charcot Triad of MS?

A

1) Scanning Speech
2) Intention Tremor
3) Nystagmus

276
Q

What are the findings of MS (pathologically)

A

Increased IgG and myelin basic protein CSF
Oligoclonal bands are diagnostic
MRI is gold standard
Periventricular plaques
Have multiple leisions seperated in space and time

277
Q

How is MS treated?

A

B interfearon
Glatiramer
Natalizaumab
Acute flares treated with IV steroids

278
Q

Acute inflammatory demyelinating polyradiculopathy?

A

Subtype of Gillian Barre syndrome
Autoimmune (destroys Scwhann cells)
Have symmetric ascending muscle weakness/ paralysis

Facial parlysis in 50% of the cases

Can have autoimmune dysregulation (cardiac, hypertension, hypotension)

Majority will recover completely after weeks and months

279
Q

What are findings with acute inflammatory demylinating polyradiculopathy?

A

Increased CSF protein
Normal cell count
Increase protein causing papilledema

280
Q

What are causes of acute inflammatory demylinating syndrome?

A 
Infections (Campylobacter jejuni, viral) 
(may be due to autoimmune mimicry) 
May require respiratory support 
Plasmapheresis 
IV immunoglobulins 
No role for steroids
281
Q

Acute dessiminated encephalomyelitis?

A

Multifocal, periventricular inflmmation and demylination after infection or vaccination (presents with altered mental status)

282
Q

Charcot-Marie-Tooth disease?

A

Hereditary motor and sensory neuropthy
Progressive
The proteins involved in the structire and function of periphereal nerves of the myelin sheath
Usually autosomal dominent

283
Q

Krabbe disease?

A

Autosomal recessive due to deficiency of galactocerbrosidase
Buildup pf galatocerebroside amd psychosine destroy the myelin sheath

Findings: central and periphereal demylination with ataxia and dementia

284
Q

Progressive multifocal leukoencephalopathy?

A

Demylination of CNS due to destruction of oligodendrocytes

Seen in 2-4% of AIDS patients

Reactivation of latent JC infection

Rapid progrression, usually fatal

Increase risk associated with natalizumab, rituximab

285
Q

Adenoleukodystrophy?

A

X linked genetic disorder affecting males
Disrupts metabolism of very-long-chain fatty acids

Excessive buildup in the nervous system, adrenal glan, and testes

Can lead to long term coma/death

286
Q

Characteristics of Partial Seizures?

A

Affect a single area of the brain
Usually originate in the temporal lobe
Usually have an aura

287
Q

What is a simple, partial seizure?

A

The consciousness is left intact

288
Q

What is a complex partial seizure?

A

Impaired consciousness

289
Q

epilepsy?

A

Disorderes of recurrent seizure

290
Q

Status epilepticus?

A

Continuous or reccurrent seizures

Can result in brain injury if more then 5 minutes

291
Q

What are common causes of seizures by age?

A

Children: Genetic, infection, trauma, congenital, metabolic

Adults: tumor, trauma, stroke, infection

Elderly: stroke, tumor, trauma, metabolic infection

292
Q

What is a generalized seizure disorder?

A

Absense (petit mal) : 3Hz, no postictal confusion
Myoclonic -quick and repetitive jerks
Tonic-clonic (grand mal) alternating stiffaning and movement

Tonic: stiffening

Atonic: Drop seizures, fall to the floor (appears like fainting(

293
Q

Characteristics of Cluster Headaches?

A

Unilateral (15 minutes to 3 hour)
Repetitive brief headaches
Periorbital pain with lacrimation and rhinorrhea
May present with Horner’s syndrome

Treatment: Sumatriptan
O2
Porphylaxis: verapamil

294
Q

Tension headache ?

A

Bilateral
> 30 minutes (typically 4-6) constant
photophobia or phonophobia (no aura)

Medications:
Analgesics
NSAIDS
Amitryptilline for the chronic pain

295
Q

Migraine headache?

A

Unilateral (4-72 hours)
Pulsating with nausea, photophobia or phonophobia
May have an aura
Irritation to CN V

Treatment:
NSAIDS
Triptans
Prophylaxis: lifestyle change (sleep, exercise, diet)

Can also use:
B Blocker, Calcium Channel blockers
Amitryptiline

296
Q

What is Trigeminal neuralgia?

A

Repetitive, unilateral shooting pain in the destributin of CN V that typically lasts < 1 minute

297
Q

What is Vertigo?

A

Sensation of spinning while sedentary
Subtype of dizziness
Distinct from lightheadedness

298
Q

Periphereal vertigo?

A 
More common 
Inner ear etiology 
Semi-circular canal debris 
Vestibular nerve infection 
Meniere's disease

Positional testing: delayed horizontal nystagmus

299
Q

Central vertigo?

A 
Brain stem 
Cerebeller lesion (stroke, vestibular nuclei, posterior fossa tumor)

Findings: directional change of nystagmus, skew deviation, diplopia, dysmetria

Positional testing: intermediate nystagmus in any direction
Focal neurological testing

300
Q

Sturge-Weber syndrome?

A

Congenital non-ingerited anomaly of neural crest
Have a port sized stain on the face

Will have seizures/epilepsy, intellectual disability and episceleral hemangioma

Increased intra-ocular pressure

early onset glaucoma

301
Q

What is Tuberous Sclerosis?

A 
Harmatomas in CNS and skin 
Angifibromas 
Mitral Regrugitation 
Cardiac Rhabdomyoma 
Autosomal dominenet 
Intellecutal disability
302
Q

Neurofibromatosis?

A 
Cafe au lait spots 
Lisch nodules
Cutaneous neurofibromas 
Optic glinomas 
Pheochromocytoma 
Chromosome 17
Neurofibromas are derived from neuro crest cells
303
Q

Von Hippel-Lindau disease?

A

Hemangioblastomas (high vascularity with hyperchromic nuclei)

Retina, brainstem, cerebellum
Angiomatosis (cavernous hemangiomas in skin, mucosa, organs, bilateral renal cell carcinoma, pheochromocytomas)

304
Q

Glioblastoma?

A 
Highly malignant 
About 1 year survival 
Found in cerebral hemisphere 
Can cross the corpus callosum 
Stain astrocytes for GFAP
305
Q

Meningioma?

A

Typically beign tumor
Most often near surface of the brain and parasaggital region
Often assymptomatic (may present with seizures or focal neurological signs)

306
Q

Hemanioblastoma?

A

Often cerebeller
Associated Von Hippel-Lindau syndrome
Associated with retinal agniomas
Can produce erythropeitin (with resultant polycythemia)

307
Q

Schwannoma?

A

Cerebellopontine Angle
Usually localized to CN 111
Bilateral schwannoma found in NF-2
Resection or Stereotactic radiosurgery

308
Q

Oligodendroglioma?

A

Relatively slow growing
Most often found in frontal lobes
Often calcified

309
Q

Pituitary adenoma?

A

Most commonly pituitary prolactinoma or non functioning adenoma

Bitemporal hemianopia due to pressure of the optic chasm (shows normal visual field due to pressure on optic chasm)

Hyper or hypopitiotarism are sequlae

Hyperplasia of a single type of endocrine cell in the pituitary

310
Q

Pilocytic astrocytoma?

A

Well circumscribed
Posterior fossa
Rosenthal fibers; eosinophile, corkscrew, cystic
Benign, good prognosis

311
Q

Medulloblastoma?

A

Highly malignant cerebeller tumor
Primitive neuroectodermal tumor
Can be in 4th ventricle
Can cause non communicating hydrocephalus
Can send drop metastatsis in the spinal chord

312
Q

Ependymona?

A

Ependymal cell tumors found in the 4th venticle
Can cause hydrocephalus
Poor prognosis
Characteristic perivascular rosettes

313
Q

Craniopharyngioma?

A

Childhood tumor
May be confused with pituitary Adenoma (both cause bitemperal hemianopia)

Most common supratentorial tumor

Dervived from remmanents of Rathke pouch

314
Q

Pinealoma?

A

Tumor of the pineal gland
Can cause Parinaud syndrome (compression of tectum leading to vertical gaze palsy)

Obstructive hydrocephalus
Precocious pubert in males due to B-HCG production
Histoogically similar to germ cell tumors (testitcular seminoma)

315
Q

Cingulate herniation?

A

Under falx cerebri (compresses the anterior cerebral artery)

316
Q

Transtentorial (central herniation)

A

Caudal displacement of the brainstem
Rupture of the paramedian basilar artery branches
Duret hemorages, usually fatal

317
Q

Uncal herniation?

A

Uncus: median temporal lobe
Compression ipsilateral CN III (blown pupil, down and out gaze)

Ispilateral PCA (contralateral homonymous hemaniopia with macualar sparing

Contalateral crus cerebri at the Kernohan notch (ipsilateral paraisis, a false location sign

318
Q

Cerebeller tonsilar herniation into the foramen magnum?

A

Coma and death result when these herniations compress the brain stem

319
Q

Glaucoma drugs?

A

Epinephrine (alpha 1) decrease aqeous humor synthesis via vasoconstriction

Decrease aqueous humor synthesis

Adverse effects: mydraisis (alpha 1) do not use in closed angle glaucoma

Blurry vision

Hyperemia

Foreign body sensation

Ocular allergic reactions

Ocular pruritis

B blockers (timolol, betaxolol, carteolol)

Decrease in aqueous humor synthesis
adverse effects: no pupillary or vision changes

Diuretics:

Acetazolamide: decrease in aquaous humor synthesis via inhibition of carbonic anhydrase

No pupillary or vision changes

Direct (pilocarpine carbachol) : increase outflow of aqeous humor via contraction of cilary muscle and opening of trabecular meshwork

Use pilocarpine in emergencies (very effective at opening meshwork) into canal of Schlemm

Adverse effects: Miosis (contraction of pupillary sphincter muscles and cytoplasm)

Prostaglandin (bimatoprost), latanoprost
Increase in outflow of aqueous humor

320
Q

What are opiod analgesics ?

A

Morphine, fentanyl, codiene, loperamide, methadone, meperidine, desrromethorphan

Mechanims: agonsit at opiod receptors (B-endorphn, enkephalin) to modulate synaptic transmission

Inhibit release of Ach

Adverse effect: addiction, respiratory suppression, constipation, miosis

Toxicity treated with naloxone or naltrexone (opiod recpetor antagonist)

321
Q

What is pentazocine?

A

K-opiod receptor agonist and u-opiod receptor

Used for analgesia for moderate to severe pain

Adverse effects: Opiod withdrawl symptoms (if patients is also taking full opiod antagonsit

322
Q

Butorphanol?

A

K-opiod receptor agonist an u-opiod receptor partial agonist

Produces analgesia

Clinical use: severe pain, causes respiratory depression

Adverse effect: Can cause opiod withdrawl symptoms if patient is taking full opiod agonist (competition for opiod receptors, overdose not easily reversed with naloxone

323
Q

What is tramadol?

A

Mechanism: very weak opiod agonist, also inhibits 5-HT and norepinehprine uptake (works on multiple neurotransmittors)

Clinical use: Chronic pain

Decreases Serotonin syndrome

324
Q

Ethosuximide (uses, mechanism, sideeffects)

A

Used in absense

Mechanism: blocks thalamic T-type Ca channels

Side effects: GI, fatigure, headache, urticaria, Steven-Johnson

325
Q

Benzodiazepines?

A

For status epilepticus
Increase of GABA action
Side effects: sedation, tolerance, dependence, respiratory depression

326
Q

Phenytoin ?

A

Simple, complex, tonic-clonic seizures

Blocks Na 2+ channels

Neurologic: nystagmus, diplopia, ataxia, sedation, periphereal neuropathy

Hirutism
Steven’s Johnson syndrome
gingival hyperplasia
DRESS syndrome

Osteopenia
SLE-like syndrome

Hematologic: megloblastic anemia

Reproductive: teratogenesis

327
Q

Carbamazepine?

A

Simple, complex and tonic-clonic seizures

Blocks Na 2+ channels

Diplopia
Ataxia
Blood dyscrasias
agranulocytosis 
Aplastic anemia 
Liver toxicity
328
Q

Valporic acid?

A

Simple, Complex, Tonic-Clonic

Increases Na+ channel inactivation
Increase in GABA concentration (inhibits GABA transaminase)

GI distress, rare but fatal 
Hepatotoxicity 
pancreatitis
Neural tube defects 
Tremor
Weight gain 
Contra-indication in pregnency

Can also be used for myoclonic seizures, bipolar disorder, migraines

329
Q

Vigabatrin?

A

for simple and complex seizures

Increase GABA by irreveribiliy inhibiting GABA transaminase

330
Q

Gabapentin?

A

Simple and complex seqizures

Primarily inhibits voltage activated CA 2+ channels, designed as GABA analog

331
Q

Topiramate?

A

Simple and Complex seizures
Blocks Na 2+ channes
Increase GABA action

Side effects: Sedation, mental dullness, kidney stones, weight loss

332
Q

Lamotrigine?

A

Simple, complex, tonic-clonic, absense,

Mechanism: blocks voltage gated Na+ channels

Adverse effects: Stevens-Johnspm syndrome

333
Q

Levetiracetam?

A

Simple
Complex
Tonic-clonic

Unknown mechanism

May modulate GABA and glutamate release

334
Q

Tiagabine?

A

Simple
Complex

Increase GABA by inhibiting reuptake

335
Q

What are uses of barbiturates?

A

Example: Phenobarbitol, pentobarbitol, thiopental, secobarbital

Mechanism: facilitate GABA, increase duration of Cl-
thus decreasing neuron firing

Clinical uses: sedation for anxiety, seizures, insommia, induction of anesthesia

Adverse effects: overdose treatment is supportive

336
Q

What are the uses of barbituates?

A

Daizepam, loazepam, traizolam, temazepam

Mechanism: facilitate GABA (increase frequency of Cl- channel opening)

decrease of REM sleep

Have long half lives

NOTE: all benzos bind on GABA receptor which is ligand gated CL

Clinical use:

Anxiety, Spasticity, status epileticus, eclampsia, detoxification, night terrors, sleepwalking, general anesthesia, hypnotic insommnia

Adverse effects:
Dependence, CNS depression (withETOH)

Overdose treated with flumazenil (can precipitate seqizures by causing acute benzodiazepine withdrawl

337
Q

Non benzodiazepine hypnotics?

A

Zolpidem, zaleplon,
zoplicone

Mechanism: act via BZ1

Clinical use: Insomnia

Adverse effects: ataxia, headaches, confusion, short duration (metabolism by liver enzymes)

modest psychomotor depression and few amnestic effects

338
Q

what are characteristics of anesthetsic drugs?

A

CNS must be lipid soluable and cross the blood-brain barrier

Can be actively transported

339
Q

What characteristics of drugs allow for rapid induction ?

A

Decrease soluability within the blood

However, increased soluability in lipids will increase the potency (1/MAC)

MAC = minimal alveolar conctration (of inhaled anesthestics) required to prevent 50% of subjects from moving due to noxious stimulus

340
Q

Comment on potency of Nitrous oxide and halothane?

A

Nitrous oxide has decreased blood and lipid soluability and thus fast induction and low potency

Halothane: has high lipid and blood solubility, slow induction, and high potency.

341
Q

Which are the inhaled anesthetics?

A

Deslurane, halothane, enflurane, sevoflurane, methoxyflurane

effects: mechanism unknown
effects: myocardial depression, respiratory depression, nausea, emesis, increase cerebral blood flow

Adverse effects: hepatoxicity, nephrotoxicity, proconvulsant, expansion of trapped gas in the body cavity

Malignany hyperthermia

342
Q

Describe malignant hyperthermia?

How to treat?

A

rare, life threatening condition in which inhaled anesthetetics or succinycholine induce fever and severe muscle contractions

Susceptibility is inherited as autosomal dominant with variable penetrance

Can be due to mutations in voltage sensitive ryanodine receptor cause increase in Ca 2+ from sarcoplasmic

Treat with: dantrolene

343
Q

Intravenous anesthestics: barbituates (thiopental)?

A

High potency
High solubility
Rapid entry into the brain
Used for induction of anesthesia and short surgical procedures
Effect terminated by rapid distribution into the tissue

344
Q

Intravenous anesthetics: midazolam

A

Used for endoscopy (can use with gaseous anesthetics and narcotics)

can cause severe postoperative respiratory depression

Decrease in BP (treat overdose with flumenzanil)

Antegrade amnesia

345
Q

Intravenous anesthestics: ketamine (arycyclohlamines)

A

PCP analogs that act as disassociative anesthestics
Blocks NMDA receptors
Cardiovascular stimulants
Cause deterioration, hallucination, bad dreams
Increase cerebral blood flow

346
Q

Propofol ?

A

Used for sedation in ICU
Rapid anesthsia induction
Short procedures
Less postoperative nausea then thipental

347
Q

Opiods as anesthestics?

A

Morphine, fentanyl, and other CNS depressants during general anesthesia

348
Q

What are the two classes of local anesthetics?

A

Esters: prociane, cocaine, tetracaine,

Amides: lidocainem mepivaine, buvicaine

349
Q

How do local anesthetics work?

A

Block Na channels

350
Q

why are they given with vascoconstrictors?

A

To enhance local action, and decrease bleeding, increase anesthesia, and decrease systemic concentration

351
Q

What happens when there is infected tissue?

A

acidic tissue, prevents the alkaline anesthetic from penetrating, and therefore you need more.

352
Q

How does the nerve blockade work?

A

small fibers, more then large fibers

myelinated fibers, before non myelinated

size is more important then myelination

353
Q

what is the order of loss for local anesthetics?

A

pain, then temperature, then touch, then pressure

354
Q

What are the side effects of local anesthetics?

A 
CNS excitation
Severe cardiovascular toxicity
Hyptertneion
Hypotension 
arrythmia 
Methemogloinemia
355
Q

Neuromuscular blocking drugs?

A

Muscle paralysis in surgery or mechanical ventilation (selective for nicotinic receptors)

Can be depolarizing

Or non -deploarizing

356
Q

example of deploarizing drug?

A

succinylocholine (strong Ach receptor agonist) produces sustained depolarization and prevents muscle contraction

Reversal of blockade:
Phase I: prolonged depolarization (no antidote)

Phase II (repolarized but blocked) reversed with cholinesterase inhibitors

Complications include: hypercalcemia, hyerpkalemia, malignant hyperthermia

357
Q

Examplses of non depolarizing drugs?

A

Tubercuranine, atracurium, mivacurium, rocuronuim Competitive antagonists

reversal of blockade: neostigmine (given with atropine) to prevent muscurininc effects such as bradycardia

358
Q

What is dantrolene?

A

mechainsm: prevents release of calcium from sarcoplasmic reticulum of skeletal muscle

Clinical use: malignant hyperthermia and neuroleptic malignant syndrome

359
Q

Balofen?

A

Atiates GABA reeptora

360
Q

Cylobenzapine?

A

Central ating skeletal musle relaxantStrutrually

361
Q

What isthe cause of Parkinson?

A

Loss of doaminergic neurons and excess cholinergic activitiy:

Bromocriptne
Amantadine
Levodopa with carbidopa
Selegiline

362
Q

How to dopamine agonist work?

A 
Ergot (Bromocriptine) 
Non ergot (preferred) pramipexole, ropinirole
363
Q

What increases dopamine availability?

A

Amantadine (increase dopamine release) and decrease dopamine reuptake

toxicity results in ataxia and reticularis

364
Q

What are agents that increase L-dopa availability?

A

Agents prevent periphereal pre-BBB
L-dopa degeneration (block peripheral conversion of L-DOPA to Dopamine by inhibiting Decarboxylase
Increase L-Dopa entering CNS
Increase Central L-Dopa available for conversion to dopamine

365
Q

How to prevent dopamine breakdown?

A

Agents act centrally (post BBB) to inhibit breakdown of dopamine

Selegoline blocks conversion of dopamine into DOPAC by selectvely inhibiting MAO-B

Tolcapone blocks conversion of dopamine 3 OMD by inhibiting central COMT

366
Q

How to curve excessive cholinergic activity?

A

Benztropine (anti-muscarinic, improves tremor and rigidity but has little affect on braykinesis in Parkinsons

367
Q

How does L-Dopa work?

A

Combination of levodopa/carbidopa

L- Dopa (levodopa) Increase level of dopamine in the brain
Unlike dopamine, it can cross the blood-brain barrier
Converted to dopa-carboxylase in the CNS to dopamine

Carbidopa periphereal DOPA (decarboxylase inhibitor) is given with L-Dopa in the brain to limit periphereal side effects

Sideeffects:

Arrythmias from peripheral formation of catecholamines
Long term use can have dyskinesia

368
Q

What are the mechanisms of selegilline, rasagiline?

A

Mechanism: selectively inhibit MAO-B (metabolize dopamine, increase dopamine availability

Clinical use: adjunctive agent to L-Dopa in treatment of Parkinsons

Side effect: May enhance adverse effects of L-Dopa

369
Q

Alzheimers drug, memantine?

A

Mechanism: NMDA receptor agonist (helps prevent excitotoxiciy) mediated by Ca 2+

Adverse effects: dizziness, confusion, hallucinations

370
Q

Alzheimers drugs donepezil, galantamine, rivastigmine, tacrine?

A 
Acetylcholine (AChe inhibitors) 
Adverse effect (nausea, dizziness, insomnia)
371
Q

What are huntington drugs?

A

Tetrabenzine and reserpine

Inhibit the vesicular monamine tranporter (VMAT) decrease dopamine vesicle packaging and release

Haloperidol : D2 receptor antagonist

372
Q

Riluzole?

A

Treatment of ALS that increases survival by decreasing glutamte excitotoxicity via unknown mechanicm

(Lou Gehig’s disease)

373
Q

What are triptans used for?

A

Example is sumatriptan.

%-Ht agonist (inhibits trigeminal nerve activation)
Prevents vasoactive peptide release

Clinical use: Acute mirgraine and cluster headache attacks

Adverse effects: Coronary vasospasm (therefore contraindicated in patients with CAD or Prinzmetal angina)

Can result in mild paresthesia

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