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
What are portions of the peripheral nerves?
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)
26
Where are the following neurotransmittors found? | What happens in their clinical diseases?
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
27
Functions of the hypothalamus?
Thirst and water balance Adenohypophysis (regulates anterior pituitary) Neurohypophysis: Hunger Autonomic regulation Temperature regulation Sexual urges
28
What does the lateral area do?
Hunger | destruction will lead to anorexia
29
Function ventromedial area?
Satiety Destruction (craniopharyngioma)
30
Function of anterior hypothalamus?
cooling | parasympathetic
31
Function of posterior hypothalamus?
Heating | Sympathetic
32
Function of suprachiasmatic nucleus?
Circadian rhythm
33
What controls sleep?
Circadian rhythm (by the supracharismatic nucleus)
34
What hormones are released by nocturnal controls?
Norepinephrine, pineal gland, melatonin,
35
What are the stages of sleep physiology?
REM and non REM | REM occurs every 90 minutes and duration of REM increases with release of ACh
36
What substances are associated with decrease REM?
ETOH, benzo, barbiturates
37
How to treat bedwetting?
Sleep enuresis, treated with desmopressin (ADH analog) preferred over imipramine
38
What medication is useful for night terrors and sleep walking?
Benzodiazepines
39
What are the ECG waveforms for the different stages of sleep?A
Awake (eyes open, alery, active mental concentration) Beta waves Awake (eyes closed) alpha
40
What are stages of NON-REM sleep?
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
41
What is REM sleep?
``` Loss of motor tone Increase in O2 use Variable pulse pressure Penile and clitoral tumescence May serve memory ```
42
Use of Ventral postero-lateral nucleus ?
Input: spinothalamic and dorsal columns Senses Pain, temperature, touch, vibration and proprioception Destination: somatosensory cortex
43
Use of the ventral-postero medial nucleus?
Trigeminal and gustatory pathways Responsible for face sensation and taste Destination: primary somatosensory cortex
44
Lateral geniculate nucleus?
CN 2 Responsible for vision Destination: Calcarine sulcus Lateral=light
45
Medial geniculate nucleus?
Input: superior oliver and inferior colliculusof tectum Senses:
46
Ventral lateral nucleus?
Input: basal ganglia, cerebellum Senses: Motor Destination: Motor Cortex
47
What is the limbic system?
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)
48
What happens when the following dopaminergic pathways are damaged? Mesocortical Mesolimbic Nigrostrial Tuberoiunfundibular
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
49
Function of the cerebellum?
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
50
Lateral lesions of the cerebellum?
Voluntary movement of extremitires with propensity to fall toward the injured, ipsilateral side
51
Medial leisions?x3
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
52
Functions of Basal Ganglia?
Recieves cortical input (provides negative feedback to cortex to modulate movement)
53
What does striatum affect?
putamen (motor) + caudate (cognitive)
54
What does lentiform affect?
Putamen + globus pallidus
55
Movement disorders: athetosis?
Slow, writhing movements of the fingers | Lesion within the Basal gangla (huntingtons)
56
Movement disorders: Chorea?
Sudden, jerky, purposeless movement | Basal ganglia lesion
57
Essential tremor?
High frequency tremor with sustained posture (outstrected arms) worsened with movements or when anxious
58
Hemiballismus?
Sudden, wild flailing of 1 arm, +/- ipsilateral leg | Usually due to contralateral subthalamic nucleus
59
Intention tremor?
slow, zigzagging motion when pointing/extending toward a target Due to cerebellar dysfunction
60
What is myoclonus?
sudden, brief, uncontrolled muscle contraction | Will have jerks, hiccups, common abnormalities in the renal and liver failure
61
What is a resting tremor?
Uncontrolled movement of the distal appendages Tremor is allreviated by intentional movement Occurs as a pill-rolling tremor (Parkinsons)
62
Characteristics of parkinson's disease?
Degenerative disorder for the CNS associated with Lewy bodies Loss of dopaminergic neurons ``` Tremor Rigidity Akinesia Postural instability Shuffling gait ```
63
Characteristics of Huntington's disease?
``` Autosomal dominent Symptoms manfest between 20-50 years of afe Chloriform movemebts agression Depression Dementia Increase dopamine Decrease dopamine Decrease GABA Decrease Ach ```
64
What is aphasia?
Inability to understand, speak, read and write | higher learning language deficit
65
Dysarthria?
Motor inability to speak (movement deficit)
66
Broca aphasia?
Non fluent speech Comprehension is intact Reptition is impaired Due to inferior frontal gyrus of frontal lobe
67
Wernicke's aphasia?
Speech fluidity: fluent Comprehension: impaired Repitition: impaired Wernicke is wordy but makes no sense
68
Conduction aphasia?
Fluidity: fluent Comprehension: intact Repeatition Impaired Caused by damage to the arcuate fasciculus
69
Global aphasia?
Fluidity: non Comprehnesion: impaired Repitition: impaired Region: arcuate fasciculus (Broca and Wernicke's areas are affected)
70
Transcortical motor aphasia?
Fluidity: nonfluent Comprehension:intact Repetition : Intact Affects the frontal lobe around Broca (but Broca area is spared)
71
Transcortical sensory apahsia?
Fluidity: fluent Comprehension: impaired Repitition: Intact Affects the temporal lobe around the wenicke area, but the wernicke is spared
72
Transcortical mixed
Broca and Wernicke area and arcuate fasciculus remain intact, but surrounding watershed areas are affected
73
Leisions of the brain associated with amygdala?
Kluver-Bucy syndrome (uninhibited behavior: hyperphagia, hypersexuality, hyperorality) Associated with HSV-1 encephalitis
74
Lesions to the frontal lobe?
Disinhibition and deficits in concentration | Re-emergence of primitive reflexes
75
Leisions of nondominent parietal cortex?
Hemispatial neglect syndrome (agnosia of contralateral side of the world)
76
Lesions of the dominenet parietal cortex?
Agraphia, acalculia, finger agnosia, left-right disorientation
77
Lesions of reticular activating system (midbrain)
Reduced levels of arousal and wakefulness
78
Mamillarybody lesions?
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
79
Lesions of the of the basal ganglia?
Tremor at rest Chorea Athetosis Parkinsons Disease Huntington's disease
80
Lesions of the Cerebeller hemisphere?
``` Limb tremore limn atazia lose of balance Ipsilateral deficits Fall toward side of the lesions ``` Associated with chronic ETOH use
81
Lesions of the cerebellar vermis?
Truncal ataxia Dysarthria Vermis is centrally located
82
Lesions of the subthalamic nucleus?
Contralateral hemiballismus
83
Lesions of the hippocampus (bilateral)
Antegrade amnesia (inability to make new memories)
84
Paramedian pontine reticular formation leisions?
Eyes that look away from the side of the leision
85
Frontal eye field leisions?
Eyes look toward the leisions
86
How does cerebral brain perfusion occur?
Relies on autoregulation (driven by PCO2) | When there is severe hypoxia then (PO2 will modulate perfusion)
87
what does cerebral perfusion rely upon?
The gradient between the mean arterial pressure (MAP)and the ICP Decrease in BP or increase in ICP leads to decrease cerebral perfusion pressure
88
What is therapeutic hyperventilation?
``` Decrease PCO2: leads to vasoconstriction decrease cerebral blood flow Decrease in ICP Used to treat acute cerebral edema (due to stroke) ```
89
What is the CPP calculation?
CPP= MAP-ICP | If the CPP is zero, there is no cerebral perfusion, leading to brain death
90
What is area of distribution for anterior cerebral artery?
Anteromedial surface
91
Area of distribution of middle cerebral artery?
Lateral surface of the brain
92
Area supplied by the posterior cerebral artery?
Posterior and inferior surfaces
93
What are the watershed areas?
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
94
what is the circle of Willis?
Anterior cerebral artery, connects to middle cerebral artery to the posterior cerebral artery, to the internal carotids
95
Stroke in the middle cerebral artery?
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
96
Lesion of the anterior cerebral artery?
Motor and sensory lower limb | Contralateral paralysis and sensory loss (lower limb)
97
Lenticulostriate artery?
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
98
Lesions of the anterior spinal artery?
``` Contralateral paralysis (upper and lower limbs) Decreased contralateral proprioception Ipsilateral hypoglossal dysfunction (tongue deviates ipsilaterally) ```
99
Medial medullary syndrome?
Caused by infarct of the paramedian branches of Anterior spinal artery or the vertebral arteries.
100
Lesions of the posterior inferior cerebral artery
``` 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 ```
101
What is the laterl medullary (Wallenberg syndrome)?
Nucleus ambiguous effects are specific to posterior inferior cerebellar artery "Don't pick a horse (hoarseness) that can't eat (dysphagia)
102
Lesions of the anterior, inferior cerebellar artery?
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 ```
103
Lesions of the basal artery?
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
104
Lesions in the posterior cerebral artery?
Area of leision: occipital cortex and visual cortex | Leads to contralateral hemianopia with macular sparing
105
Lesions of the middle cerebral artery?
Rupture may cause ischemia in the MCA distribution (contralateral upper extremity, facial hemiparesis and sensory deficits)
106
Central post stroke pain syndrome?
Neuropathic pain due to thalamic lesions Initial parestheisis followed in weeks to months by allodynia and dysesthesia Occurs in 10% of stroke patients
107
Epidural hematoma?
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
108
Subdural hematoma?
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
109
Subarachnoid hemorrhage?
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
110
How to prevent transformation of subarachnoid hemorrhage from an ischemic stroke?
Give nimodipine
111
What is intraparenchymal hemohage?
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
112
When does irreversible damage to the brain occur?
After 5 minutes of hypoxia
113
What are regions most vulnerable for damage in the brain?
Hippocampus Neocrotex Cerebellum Watershed areas
114
What type of test is required for a stroke?
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
115
What are the three types of ischemic stroke?
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
116
When can TPA be used for stroke?
If within 3-4.5 hours of onset | No risk of hemorrage
117
How to reduce the risk of stroke?
``` ASA and Plavix Optimum control of blood pressure Control blood sugar Control lipids Treat A fib ```
118
Definition of TIA?
Brief, reversible episode of neuro dysfunction without acute infarct (MRI -) usually resolves within 15 minutes
119
What are dual venous sinuses?
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
120
What is a venous sinus thrombosis?
Presents with signs/symptoms of increase ICP | Headache, seizure, focal neurological deficits.
121
what conditions are associated with Venous sinus thrombosis?
Hypercoagulable states (pregnancy, OCP, factor V Leiden)
122
Idiopathic intracranial HTN? Symptoms? Risk?
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
123
What does hydrocephalus mean?
Increase in CSF volume with ventricular dilation and increase in ICP
124
What is communicating hydrocephalus>
Decrease CSF asbsorption by arachnoid granulations | Increase in ICP leading to pailledema and herniation
125
What is normal pressure hydrocephalus?
``` Elderly Idiopathic CSF pressure only periodically elevated Expansion of the ventricles Distorts fibers of the corona radiata ```
126
What are the triad of normal presssure hydrocephalus?
Urinary incontinence Ataxia Cognitive dysfunction
127
What is the cause of non communicating (obstructive hydrocephalus)
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
128
What are conditions of hydrocephalus mimics?
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
129
How mant spinal nerves are there?
There are 31 pairs of spinal nerves ``` 8 cervical 12 thoracic 5 lumbar 5 saccral 1 coccygeal ```
130
Where do the spinal nerves exit?
C1-C7 above the corresponding vertebraw
131
Where does the subarachnoid space extend to?
The lower border of the S2 vetebrae
132
Where do lumber puncture usually performed?
L3 and L4 or L4 and L5
133
Describe the anatomy of the spinal cord?
``` white matter on the outside Grey matter is butterfly on the inside CSF directly in the middle Venticle fissue Dorsal median sulcus ```
134
what are the parts of the dorsal column?
Gracile | Cuneate
135
What is the dorsal column responsible for?
Proprioception | Fine touch
136
Briefly describe the Dorsal Column Tract?
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
137
Briefly describe the spinothalamic tract?
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
138
Briefly describe the lateral corticospinal tract?
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
139
What are characteristice of lower moter neuron leision vs upper motor neuron?
``` 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 ```
140
Characteristics of Poliomyelitis and Werdnig-Hoffmann disease?
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
141
Characteristics of amyotrophic lateral sclerosis?
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
142
Characteristics of complete occulsion of the anterior spinal artery?
Spares dorsal column | Anterior spinal artery is a watershed area.
143
Charactersitics of Tabes dorsalis?
Caused by 3 syphilis | Degeneration or demyelination of dorsal columns and roots leading to ataxia and poor coordination
144
Characteristics of Syringomyelia?
Syrinx can expand and damage anterior commisure of spinothalamic tract Bilateral loss of pain and temperature sensation in cape-like distribution
145
Characteristics of Vitamin B deficiency?
Sub acute degeneration (demyelination of Spinocerebeller tracts), lateral corticospinal tracts, and dorsal column. Leads to ataxia, paresthesia, impaired position/vibration
146
What is poliomyelitis?
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
147
What is Friedereich's ataxia?
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
148
What is Brown-Sequard syndrome?
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
149
dermatome C2?
Posterior half of the skull cap
150
dermatome of C3?
High turtleneck shirt
151
dermatome of C4?
Low coller shirt
152
dermatme of C6?
arm and includes the thumbs
153
T4?
at the nipple
154
T7?
at the xiphoid process
155
T10?
at the umbolicus
156
L1?
At the inguinal ligametn
157
L4?
Includes the kneecaps
158
S2, S3, S4?
erection and sensation of penile and anal zones
159
Where does diaphgram and gallbladder pain refer?
Referred pain to the shoulder via the phrenic nerve
160
reflexes of the biceps?
C5 nerve root
161
Reflexes of the triceps?
C7
162
Reflexes of the patallea?
L4
163
Reflexes of the achilles?
S1 nerve root
164
when do primitive reflexes occur?
Inhibited by mature developing frontal lobe Can reemerge if the adult has frontal lobe leisions Leads to loss of inhibition of the reflexes
165
Moro reflex?
Hang on for life | Abduct and extend arms when startled (and then draw together)
166
Rooting reflex?
Movement of the head toward one side if cheek or mouth is stroked
167
Sucking reflex?
Sucking response when roof of the mouth is touched
168
Palmar reflex?
Curling fingers if palm is stroked
169
Plantar reflex?
Dorsiflexion of large toe and fanning of other toes with plantar stimulation Babinski sign: presence of this reflex in an adult (UMN)
170
Galant reflex?
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
Which cranial nerves are above the pons?
I II III IV
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Cranial nerves in the pons?
V V1 V11 V111
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Cranial nuclei that are medial?
III IV VI X11
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function of the pineal gland?
Melatonin secretion | Circadian rhythms
175
Superior colliculi?
Conjugate vertical gaze center | note, your eyes are above your ears, and the superior colliculus are above the inferior colliculus..ears
176
Inferior colliculi?
Auditory
177
Parinaud syndrome?
Paralysis of conjugate vertical gaze due to leision of superior colliculli (stroke, hydrocephalus
178
Cranial nerve I?
Olfactory
179
Cranial nerve II
Optic
180
Cranial nerve III
Oculomotor (eye movement), pupillary constriction, accomodation
181
Cranial nerve IV?
Trochlear | eye movement
182
Cranial nerve V?
Trigeminal | Mastication, facial sensation (opthalmic, maxillart, mandibular, diviison) somatosensation of anterior 2/3 of the tongue
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Cranial nerve VI
Abducens (eye movement)
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Cranial nerve VII
``` Facial movement Taste from anterior of the 2/3 of the tongue lacrimation salivation eyelide closing Auditory volume ```
185
Vestibulocochlear VIII?
Hearing and balance
186
Glossopharyngeal IX?
Taste and sensation from posterior 1/3 tongue, swallowing, salivation (parotid gland) Monitoriing carotid body, sinus, chemo and baroreceptors
187
Vagus X?
Taste from supraglottic region Swallowing Soft palate elevation talking, coughin, parasympathetics to thoracoabdominal viscera
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Accessory XI
Head turning, shoulder shrugging, SCM, trapezius
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Hypoglossal XII
Tongue movement
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What are the vagal nuclei *nucleus solitarius*?
Responsible for visceral sensory information (taste, baroreceptors, gut distention) Cranial nerve VII, IX, X
191
Nuclue ambigous?
Motor innervation of the pharynx, larynx, upper esophagus | IX, X, XI
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Dorsal motor nucleus?
Sends autonomic parasympathetic fibers to the heart,lung, and upper GI
193
Corneal nerve reflex?
Afferent: V1 opthalmic Efferent:V2 (temporal branch)
194
Lacrimation reflex?
``` Afferent V1 (loss of V1 does not preculude emotional tears) Efferent: V11 ```
195
Jaw jerk reflex?
Afferent: V3 (sensory-muscle spindle from masseter) Efferent: motor-masseter
196
Pupillary reflex?
Afferent II | efferent: III
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Gag reflex?
Afferent IX | Efferent X
198
CN 5 lesion?
Jaw deviates toward the side of the leision due to unopposed force from the opposite ptergoid muscle
199
CN X lesion?
Uvula deviates awat from the side of the leision (weak side collapses_
200
CN X1 lesion?
weakness turning head to contralateral side of the leision (SCM)) shoulder droop on side of lesion (trapezius)
201
CN XII leision?
LMN leision (tongue deviates toward the side of the leision) lick your wounds
202
What are the mastication muscles?
Masseter Temorarlis Medial pterygoid
203
Facial nerve leision (upper motor neuron)
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
Lower motor neuron leision?
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
Clinical syndrome of CN VII leision?
Causes partial or complete loss of function depending on location or severity of the leision Can cause partial or complete loss of function
206
What is Bell's palsy?
Caused by Lyme diseas, herpes, herpes zoster, sarcoidosis trauma, DM
207
What is treatment of Bell's palsy?
Corticosteroids Acyclovir Most have gradual return of function
208
What are cavernous sinus? | What is cavernous sinus syndrome?
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
What is the outer ear?
visible portion (pinna) includes auditory canal eardrum Transfers waves via vibration of the eardrum
210
What is the middle ear?
Air filled space with three bones, ossicles, malleus, incus, stapes Ossicles conduct and ampligy sound from eardrum to inner ear
211
what is the inner ear?
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
Where is low frequency heard?
Apex near the helicotrema
213
Where is high frequency heard?
At the base of cochlea
214
What is conducive hearing loss?
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
What is sensorineural hearing loss?
``` Rhine test (air more then bone) NORMAL Weber test (localized to the affected ear) ```
216
What is noise induced hearing loss?
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
Cholestetoma?
Overgrowth of desquamated keratin debris within the middle ear This can lead to conductive hearing loss
218
What is the pathway of aqueous humor?
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
How to decrease aqueous humor?
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
Hyperopia?
eye too short for refractive power of cornea and lens | (light focused behind the retina
221
Myopia?
eye too long for refractive power of the cornea and lens (focused in front of the retina)
222
Astigmatism?i
abnormal curvature of the cornea, with refactive power at different axis
223
Presbyopia?
Age related impaired accomadation (diffculty focusing on near objects due to decreased lens elasticity
224
Characteristics of cataract?
Painless, bilateral opacification of the lens Results in decrease of vision Increased with age, smoking, ETOH, sunlight exposure DM Trauma Infection
225
What are congential causes of catacts?
``` TORCH (rubella) Marfan sundrome Alport Syndrome Myoptonic dystrophy Neurofibromatosis 2 ```
226
What is glaucoma? What are the treatment?
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
Open angle glaucoma?
Increase with age Increase with African American race Family history More common in US
228
what are secondary causes of glaucoma?
Blocked trabecular meshwork from WBC (uvetis) RBC (vitroud hemorrage) Retinal detachement
229
What is closed angle glaucoma?
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
What are secondary causes of closer or narrow angle glaucoma?
Hypoxia from retinal disease (DM, vein occlusion) | Induces vasoproliferation in iris, that contracts angle
231
What is chronic vs Acute angle glaucoma?
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
Characterstics of conjunctivitis?
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
What is uveitis?
Inflammation of the uvea | names are specific to the location within the affected eye
234
What are the different areas?
``` Anterior uveitits Intermediate uveitisi Pars planitis Posterior uveitis Chorioditis or retinitis ```
235
What is a hypopyon?
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
Characteristics of age-related macular degeneration?
Degeneration of the macula (central area of retina) | Causes distortion and eventul loss of vision
237
What is dry macular degeneration?
Dry: nonexudative > 80% depositions of yellow extracellular material in and between Bruch membrane and retinal pigment
238
what is wet macular degeneration?
Rapid loss of vision due to bleeding 2nd to choroidal neovascularization Treat with anti-VEGF (injections, ranibizumab)
239
What is diabetic retinopathy?
Neoproliferative (damaged capillaries, leak blood) Lipids and fluids seep into the retina Can lead to hemorrages.
240
What is retinal vein occlusion?
Blockage of central or branch retinal vein due to compression from nearby arterial atherosclerosis Leads to retinal hemorrhage and venous engorgement and edema
241
What is retinal detachement?
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
What causes retinal detachement?
Retinal breaks Diabetic traction Inflammatory effusions Visualized on fundoscopy
243
Breaks are more common in which ?
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
What is central artery occlusion?
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
What is Retinitis pigmentosa?
Inherited retinal degeneration Painless, progressive vision loss, starting with night blindness Bone spicule shaped deposit arund macula
246
What is retinitis?
Retinal edema and necrosis (leading to scar) Often viral *CMV, HSV, VSV) Can be bacterial or parasitic
247
what is papilledema?
Optic disc swelling (usually bilateral) due to increased ICP Enlarged blind spot and elevated optic disc with blurred margins
248
What is responsible for pupillary control?
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
what is the pupillary light reflex?
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
What is responsible for mydriasis?
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
What is a Marcus Gunn Pupil?
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
What is Horner's syndrome?
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
What are the conditions associated with the Horner syndrome?
Pancoast tumore Brown- Sequrd syndrome Late stage syringmyelia
254
What are the muscles of the eye?
``` Superior rectus muscle Lateral rectus muscle Inferior oblique muscle (inferior rectus muscle) Medial rectus muscle Trochlea Superior oblique muscle ```
255
What is the formula to remember what nerves innervate which muscle?
LR6 SO4 R3 Lateral rectus CN 6 Superior Oblique CN 4 Rest: CN 3
256
What affects CN 3 (motor and parasympathetic output)?
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
What is CN IV damage?
Eye move upward, particularly with contralateral gaze | And head tilt toward the side of the leision
258
CNVI damage?
Medially directed eye that cannot abduct
259
Lesion causing bitemporal anopia?
Pituitaty lesion (chiasm) Defect normal normal \defect (Leasions on outside of both eyes)
260
Left homonymous hemaniopia?
defect - normal defect-normal
261
left upper quadrant anopia?
1/4 of both upper eyes (facing to the left) | Right temporal lesion MCA
262
Left lower quadrant anopia?
Right parital lesion, MCA
263
Left hemainopia with with macular sparing>
PCA infarct
264
Central Scotoma?
Macular Degeneration
265
what is internuclear ophtalmoplegia?
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
What are characteristics of Alzeihmers?
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
What are histological findings of Alzehiemers?
``` Widespread cortical atrophy Decrease in ach Senile plaques in the grey matter Intracranial hemorrhage (Amyloid B) Neurofibrillary tangles ```
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Characteristics of early fronto-temoporal dementia?
Early changes in personality and behavior Can have progressive aphasia May have associated disorders like parkinsonian, ALS like (UMN/LMN) degeneration
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What is Lewy body dementia?
Dementia with visual hallucinations | Has parkinson features
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Vascualar dementia?
Due to multiple arterial infarcts Step wise decline in cognitive dysfunction Second most common demntia in the elderly
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Creutzfeldt-Jakob disease?
Rapidly progressing demntia Has startle myoclonus Has spongiform cortex Presence of prions
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What are other causes of dementia?
``` Syphilis HIV hypothyroidism B3 and B12 deficiency Wilson's disease Hydrocephalus ```
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What is osmotic demylination? | Causes?
``` 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
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What is multiple scleorosis?
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
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What is the Charcot Triad of MS?
1) Scanning Speech 2) Intention Tremor 3) Nystagmus
276
What are the findings of MS (pathologically)
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
How is MS treated?
B interfearon Glatiramer Natalizaumab Acute flares treated with IV steroids
278
Acute inflammatory demyelinating polyradiculopathy?
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
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What are findings with acute inflammatory demylinating polyradiculopathy?
Increased CSF protein Normal cell count Increase protein causing papilledema
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What are causes of acute inflammatory demylinating syndrome?
``` Infections (Campylobacter jejuni, viral) (may be due to autoimmune mimicry) May require respiratory support Plasmapheresis IV immunoglobulins No role for steroids ```
281
Acute dessiminated encephalomyelitis?
Multifocal, periventricular inflmmation and demylination after infection or vaccination (presents with altered mental status)
282
Charcot-Marie-Tooth disease?
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
Krabbe disease?
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
Progressive multifocal leukoencephalopathy?
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
Adenoleukodystrophy?
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
Characteristics of Partial Seizures?
Affect a single area of the brain Usually originate in the temporal lobe Usually have an aura
287
What is a simple, partial seizure?
The consciousness is left intact
288
What is a complex partial seizure?
Impaired consciousness
289
epilepsy?
Disorderes of recurrent seizure
290
Status epilepticus?
Continuous or reccurrent seizures | Can result in brain injury if more then 5 minutes
291
What are common causes of seizures by age?
Children: Genetic, infection, trauma, congenital, metabolic Adults: tumor, trauma, stroke, infection Elderly: stroke, tumor, trauma, metabolic infection
292
What is a generalized seizure disorder?
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
Characteristics of Cluster Headaches?
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
Tension headache ?
Bilateral > 30 minutes (typically 4-6) constant photophobia or phonophobia (no aura) Medications: Analgesics NSAIDS Amitryptilline for the chronic pain
295
Migraine headache?
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
What is Trigeminal neuralgia?
Repetitive, unilateral shooting pain in the destributin of CN V that typically lasts < 1 minute
297
What is Vertigo?
Sensation of spinning while sedentary Subtype of dizziness Distinct from lightheadedness
298
Periphereal vertigo?
``` More common Inner ear etiology Semi-circular canal debris Vestibular nerve infection Meniere's disease ``` Positional testing: delayed horizontal nystagmus
299
Central vertigo?
``` 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
Sturge-Weber syndrome?
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
What is Tuberous Sclerosis?
``` Harmatomas in CNS and skin Angifibromas Mitral Regrugitation Cardiac Rhabdomyoma Autosomal dominenet Intellecutal disability ```
302
Neurofibromatosis?
``` Cafe au lait spots Lisch nodules Cutaneous neurofibromas Optic glinomas Pheochromocytoma Chromosome 17 Neurofibromas are derived from neuro crest cells ```
303
Von Hippel-Lindau disease?
Hemangioblastomas (high vascularity with hyperchromic nuclei) Retina, brainstem, cerebellum Angiomatosis (cavernous hemangiomas in skin, mucosa, organs, bilateral renal cell carcinoma, pheochromocytomas)
304
Glioblastoma?
``` Highly malignant About 1 year survival Found in cerebral hemisphere Can cross the corpus callosum Stain astrocytes for GFAP ```
305
Meningioma?
Typically beign tumor Most often near surface of the brain and parasaggital region Often assymptomatic (may present with seizures or focal neurological signs)
306
Hemanioblastoma?
Often cerebeller Associated Von Hippel-Lindau syndrome Associated with retinal agniomas Can produce erythropeitin (with resultant polycythemia)
307
Schwannoma?
Cerebellopontine Angle Usually localized to CN 111 Bilateral schwannoma found in NF-2 Resection or Stereotactic radiosurgery
308
Oligodendroglioma?
Relatively slow growing Most often found in frontal lobes Often calcified
309
Pituitary adenoma?
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
Pilocytic astrocytoma?
Well circumscribed Posterior fossa Rosenthal fibers; eosinophile, corkscrew, cystic Benign, good prognosis
311
Medulloblastoma?
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
Ependymona?
Ependymal cell tumors found in the 4th venticle Can cause hydrocephalus Poor prognosis Characteristic perivascular rosettes
313
Craniopharyngioma?
Childhood tumor May be confused with pituitary Adenoma (both cause bitemperal hemianopia) Most common supratentorial tumor Dervived from remmanents of Rathke pouch
314
Pinealoma?
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
Cingulate herniation?
Under falx cerebri (compresses the anterior cerebral artery)
316
Transtentorial (central herniation)
Caudal displacement of the brainstem Rupture of the paramedian basilar artery branches Duret hemorages, usually fatal
317
Uncal herniation?
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
Cerebeller tonsilar herniation into the foramen magnum?
Coma and death result when these herniations compress the brain stem
319
Glaucoma drugs?
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
What are opiod analgesics ?
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
What is pentazocine?
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
Butorphanol?
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
What is tramadol?
Mechanism: very weak opiod agonist, also inhibits 5-HT and norepinehprine uptake (works on multiple neurotransmittors) Clinical use: Chronic pain Decreases Serotonin syndrome
324
Ethosuximide (uses, mechanism, sideeffects)
Used in absense Mechanism: blocks thalamic T-type Ca channels Side effects: GI, fatigure, headache, urticaria, Steven-Johnson
325
Benzodiazepines?
For status epilepticus Increase of GABA action Side effects: sedation, tolerance, dependence, respiratory depression
326
Phenytoin ?
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
Carbamazepine?
Simple, complex and tonic-clonic seizures Blocks Na 2+ channels ``` Diplopia Ataxia Blood dyscrasias agranulocytosis Aplastic anemia Liver toxicity ```
328
Valporic acid?
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
Vigabatrin?
for simple and complex seizures Increase GABA by irreveribiliy inhibiting GABA transaminase
330
Gabapentin?
Simple and complex seqizures | Primarily inhibits voltage activated CA 2+ channels, designed as GABA analog
331
Topiramate?
Simple and Complex seizures Blocks Na 2+ channes Increase GABA action Side effects: Sedation, mental dullness, kidney stones, weight loss
332
Lamotrigine?
Simple, complex, tonic-clonic, absense, Mechanism: blocks voltage gated Na+ channels Adverse effects: Stevens-Johnspm syndrome
333
Levetiracetam?
Simple Complex Tonic-clonic Unknown mechanism May modulate GABA and glutamate release
334
Tiagabine?
Simple Complex Increase GABA by inhibiting reuptake
335
What are uses of barbiturates?
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
What are the uses of barbituates?
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
Non benzodiazepine hypnotics?
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
what are characteristics of anesthetsic drugs?
CNS must be lipid soluable and cross the blood-brain barrier Can be actively transported
339
What characteristics of drugs allow for rapid induction ?
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
Comment on potency of Nitrous oxide and halothane?
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.
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Which are the inhaled anesthetics?
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
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Describe malignant hyperthermia? | How to treat?
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
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Intravenous anesthestics: barbituates (thiopental)?
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
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Intravenous anesthetics: midazolam
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
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Intravenous anesthestics: ketamine (arycyclohlamines)
PCP analogs that act as disassociative anesthestics Blocks NMDA receptors Cardiovascular stimulants Cause deterioration, hallucination, bad dreams Increase cerebral blood flow
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Propofol ?
Used for sedation in ICU Rapid anesthsia induction Short procedures Less postoperative nausea then thipental
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Opiods as anesthestics?
Morphine, fentanyl, and other CNS depressants during general anesthesia
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What are the two classes of local anesthetics?
Esters: prociane, cocaine, tetracaine, Amides: lidocainem mepivaine, buvicaine
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How do local anesthetics work?
Block Na channels
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why are they given with vascoconstrictors?
To enhance local action, and decrease bleeding, increase anesthesia, and decrease systemic concentration
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What happens when there is infected tissue?
acidic tissue, prevents the alkaline anesthetic from penetrating, and therefore you need more.
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How does the nerve blockade work?
small fibers, more then large fibers myelinated fibers, before non myelinated size is more important then myelination
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what is the order of loss for local anesthetics?
pain, then temperature, then touch, then pressure
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What are the side effects of local anesthetics?
``` CNS excitation Severe cardiovascular toxicity Hyptertneion Hypotension arrythmia Methemogloinemia ```
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Neuromuscular blocking drugs?
Muscle paralysis in surgery or mechanical ventilation (selective for nicotinic receptors) Can be depolarizing Or non -deploarizing
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example of deploarizing drug?
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
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Examplses of non depolarizing drugs?
Tubercuranine, atracurium, mivacurium, rocuronuim Competitive antagonists reversal of blockade: neostigmine (given with atropine) to prevent muscurininc effects such as bradycardia
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What is dantrolene?
mechainsm: prevents release of calcium from sarcoplasmic reticulum of skeletal muscle Clinical use: malignant hyperthermia and neuroleptic malignant syndrome
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Balofen?
Atiates GABA reeptora
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Cylobenzapine?
Central ating skeletal musle relaxantStrutrually
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What isthe cause of Parkinson?
Loss of doaminergic neurons and excess cholinergic activitiy: Bromocriptne Amantadine Levodopa with carbidopa Selegiline
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How to dopamine agonist work?
``` Ergot (Bromocriptine) Non ergot (preferred) pramipexole, ropinirole ```
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What increases dopamine availability?
Amantadine (increase dopamine release) and decrease dopamine reuptake toxicity results in ataxia and reticularis
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What are agents that increase L-dopa availability?
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
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How to prevent dopamine breakdown?
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
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How to curve excessive cholinergic activity?
Benztropine (anti-muscarinic, improves tremor and rigidity but has little affect on braykinesis in Parkinsons
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How does L-Dopa work?
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
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What are the mechanisms of selegilline, rasagiline?
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
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Alzheimers drug, memantine?
Mechanism: NMDA receptor agonist (helps prevent excitotoxiciy) mediated by Ca 2+ Adverse effects: dizziness, confusion, hallucinations
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Alzheimers drugs donepezil, galantamine, rivastigmine, tacrine?
``` Acetylcholine (AChe inhibitors) Adverse effect (nausea, dizziness, insomnia) ```
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What are huntington drugs?
Tetrabenzine and reserpine Inhibit the vesicular monamine tranporter (VMAT) decrease dopamine vesicle packaging and release Haloperidol : D2 receptor antagonist
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Riluzole?
Treatment of ALS that increases survival by decreasing glutamte excitotoxicity via unknown mechanicm (Lou Gehig's disease)
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What are triptans used for?
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