Neurology- Embryology and Physiology- FA Flashcards
1
Q
Notochord induces
A
Ectoderm –> neuroectoderm and neural plate
2
Q
Neural plate becomes
A
neural tube and neural crest cells
3
Q
Notocord becomes
A
nucleus pulpous of intervertebral disc in adult
4
Q
Alar plate (dorsal)
A
sensory
5
Q
Basal plate (ventral)
A
motor
6
Q
Forebrain (prosencephalon)
A
Telencephalon –> cerebral hemispheres & lateral ventricles
Diencephalon –> Thalamus and hypothalamus & third ventricle
7
Q
Midbrain (mesencephalon)
A
Mesencephalon –> Midbrain & aqueduct
8
Q
Hindbrain (rhombencephalon)
A
Metencephalon –> Pons and cerebellum & upper part of 4th ventricle
Myelencephalon –> Medulla & lower part of 4th ventricle
9
Q
Neuroectoderm becomes
A
CNS neurons, ependymal cell (make CSF), oligodendroglia, astrocytes
10
Q
Neural crest
A
PNS neurons and Schwann cells
11
Q
Mesoderm
A
Microglia (macrophages of the CNS)
12
Q
Neural tube defects
A
NEUROPORES fail to fuse (4th week); persistent connection between amniotic cavity and spinal canal
Associated with low folic acid and high alpha-fetoprotein and high acetylcholinesterase
13
Q
Spina bifida occulta
A
Most mild; failure of bony spinal canal to close, but no herniation
Usually seen at lower vertebral levels and dural is intact
Normal AFP; hair or skin dimple may be seen above region
Folic acid helps if given before the 28th day
14
Q
Meningocele
A
Meninges/ dura (but no neural tissue) herniate
Skin defect/ thinning seen on surface
15
Q
Meningomyelocele
A
Meninges and neural tissue (spinal cord/ cauda equina) herniate
Skin thin or absent
16
Q
Anencephaly
A
Malformation of anterior neural tube; no forebrain
Associated with increased AFP and polyhydramnios
Associated with Type I diabetes
Decreased risk with maternal folate supplementation
17
Q
Holoprosencephaly
A
Failure of left and right hemispheres to separate
Usually occurs during weeks 5-6
Related to mutations in Sonic Hedgehog pathway
Ranges from cleft lip/palate –> cyclopean
Seen in Patau syndrome and fetal alcohol syndrome
18
Q
Chiari II malformation
A
herniation of low-lying cerebellar VERMIS through foramen magnum with aqueduct stenosis –> hydrocephalus
Generally associated with meningomyelocele and paralysis/sensory loss at and below the level of the lesion
Typically presents at childhood (as opposed to Chiari I malformation- where tonsils herniate)
19
Q
Dandy Walker
A
Agenesis of cerebellar vermis with cystic enlargement of the fourth ventricle (fills the posterior fossa)
Associated with noncommunicating hydrocephalus (obstruction) and spina bifida
20
Q
Syringomyelia
A
Fluid filled cavity within the spinal cord (vs. syrigobulbia- medulla/ lower brainstem)
Fissures crossing in the anterior white commissure (spinothalamic tract- pain and temp) are typically damaged first
Associated with Chiari malformations, trauma, and tumors
21
Q
Syringobulbia
A
Fluid filled cavity within the medulla or lower brainstem
22
Q
Syringomyelia S&S
A
Cape-like loss of pain and temp (bilateral and affects upper extremities); with normal fine touch
Most commonly affects C8-T1
23
Q
Chiari I malformation
A
Cerebellar TONSILLAR ectopia; congenital, but usually asymptomatic in children
24
Q
Chiari I- S&S
A
Occipital headache and cerebellar dysfunction that may worsen with Valsalva
25
Tongue development- anterior
Anterior (arches 1 and 2)
Sensation: V3
Taste: VII
Motor: XII (protrudes tongue)
26
Tongue development- posterior
Posterior (arches 3 and 4)
Sensation and taste: IX (far back & uvula- X)
Motor: X (elevates posterior tongue during swallowing)
27
Tongue- Taste, Pain, and Motor (summary)
Taste: VII, IX, X
Pain V3, IX, X
Motor: X, XII
28
Neurons
Signal-transmitting cells of NS
Permanent/ do not divide
Cell bodies and dendrites IDed through Nissl staining (stains RER)
29
Wallerian degeneration
Injury to axon causes degeneration distal to injury and axonal retraction proximally (allows for regeneration of axon- if in PNS)
30
Astrocytes
```
Physical support
Repair K+ metabolism
Remove excess neurotransmitter
Component of BBB
Glycogen fuel reserve buffer
```
Astrocyte marker: GFAP
31
Microglia
Phagocytic scavenger of cells of CNS (mesodermal and mononuclear origin)- activate in response to tissue damage
HIV-infected microglia fuse to form multinucleated giant cells (HIV encephalitis)
vs. JC virus- infects oligodendrocytes
32
Myelin
Increases conduction velocity of transmitted signals (and increases space constant)
CNS: oligodendrocytes
PNS: Schwann cells
33
Nodes of Ranvier
Gaps of myelin sheath where there are high concentrations of Na+ channels (where Na+ flows into neuron)- allowing for saltatory conduction of action potentials (boosters??)
34
Schwann cells
Each cell myelinates ONE PNS axon (vs. multiple and CNS for oligodendrocytes)
Derived from neural crest
Promotes axonal regeneration
35
Guillian Barre
Causes injury to Schwann cells
36
Vestibular schwannoma (aka acoustic neuroma)
Typically located on CN VIII in internal acoustic meatus --> may extend to cerebellopontine angle
S&S: progressive hearing loss and impaired balance
Bilateral acoustic neuroma- Seen in NF Type II (affects myelination of peripheral neurons)
37
Oligodendroglia
Myelinates axons of neurons in CNS (each oligo can myelinated about 30 axones)
Seen in white matter
Fried egg appearance in histology
Injured in MS and progressive multifocal leukoencephalopathy (PML), leukodystrophies (degeneration of white matter)
38
Sensory receptors: Free nerve endings- fiber type
C- slow unmyelinated
| Adelta- fast myelinated
39
Sensory receptors: Free nerve endings- location
All skin, epidermis, some viscera
40
Sensory receptors: Free nerve endings- sensation
Pain and temp
41
Sensory receptors: Meissner corpuscles- fiber type
Large, myelinated fibers, adapt quickly
42
Sensory receptors: Meissner corpuscles- location
Glabrous skin (hairless)
43
Sensory receptors: Meissner corpuscles- sensation
Dynamic, fine/light touch, position sense, low-frequency vibration
44
Sensory receptors: Pacinian corpuscles- fiber type
Large, myelinated fibers, adapt quickly
45
Sensory receptors: Pacinian corpuscles- location
Deep skin layers, ligaments
46
Sensory receptors: Pacinian corpuscles- sensation
Deep/coarse touch, vibration, pressure
47
Sensory receptors: Merkel discs- fiber type
Large, myelinated fibers, adapt quickly
48
Sensory receptor: Merkel discs- location
Finger tips, superficial skin
49
Sensory receptor: Merkel discs- sensation
Sustained pressure, deep static touch (e.g. shapes, edges), position sense
50
Sensory receptor: Ruffini corpuscles- fiber type
Dendritic ending with capsule, adapt slowly
51
Sensory receptor: Ruffini corpuscles- location
Finger tip, joints
52
Sensory receptor: Ruffini corpuscles- sensation
Sustained pressure, slippage of objects along surface of skin, joint angle change
53
Peripheral nerve (3 layers)- endoneurium
Endoneurium: layer around a single nerve fiber, inner (inflamed in Guillain-Barre)
54
Peripheral nerve (3 layers)- perineurium
Perineurium: Permeability barrier (surrounds fascicle of nerve fibers)- must be rejoined during surgery for limb attachment
55
Peripheral nerve (3 layers)- epineurium
Epineurium: dense connective tissue that surrounds entire nerve (includes many fascicles and blood vessels)
56
Unmyelinated vs. myelinated
Unmyelinated- smaller diameters, conduct more SLOWLY
57
Examples of unmyelinated fibers
afferent neurons that conduct heat sensation, burning, visceral pain
efferent autonomic POST-ganglionic nuerons
first order bipolar sensory neurons of olfaction
58
NTs- ACh
Synthesized in basal nucleus of Meynert (superior and lateral to hypothalamus)
Decreased in Alzheimers, Huntington, and Parkinsons
59
NTs- Dopamine
Synthesized in ventral tegmentum, SNpc (midbrain)
Increased in Schizophrenia and Huntington
Decreased in Parkinsons and Depression
60
NTs- GABA
Synthesized in nucleus accumbens (basal forebrain, above hypothalamus)
Decreased in anxiety and Huntingtons
61
NTs- NE
Synthesized in locus ceruleus (pons)
Increased in anxiety
Decreased in depression
62
NTs- Serotonin
Synthesized in raphe nucleus (brainstem)
Decreased in depression and ANXIETY (which is why SSRIs are a tx for both of these condns)
Increased in Parkinsons
63
Blood brain barrier
Formed by three structures:
Astrocyte foot processes
Tight junctions between endothelial cells (non-fenestrated)
Basement membrane
64
BBB- transport
Glucose and AAs- by carrier mediated transport mechanisms
Nonpolar/ lipid-soluble: passive diffusion
Hydrophilic mcs require carrier proteins
65
Specialized regions without BBB
Area postrema- medulla (vomiting after chemo)
OVLT (vascular organ of lamina terminalis)- anteroventral third ventricular region (osmotic sensing)
Neurohypophysis/ posterior pituitary- secrets ADH
66
Vasogenic edema
Caused by destruction of endothelial cell tight junctions
Causes: infarction or neoplasm
67
Important blood/ tissue barriers
Blood-brain barrier
Blood-testes barrier
Maternal/ fetal blood barrier of placenta
68
Hypothalamus- TANHATS
Thirst and water balance
Adenohypophysis- regulates anterior pituitary
Neurohypophysis (posterior pituitary)- releases hormones produced in hypothalamus
Hunger
Autonomic regulation
Temperature regulation
Sexual urges
69
Inputs to hypothalamus (area not protected by BBB)
Supraoptic nucleus (makes ADH)
OVLT: regulate osmolarity
Area postrema: found in medulla, responds to emetics
70
Supraoptic nucleus (hypothalamus)
makes ADH
71
Paraventricular nucleus (hypothalamus)
makes oxytocin
72
Neurophysins
Carry ADH and oxytocin down axons to posterior pituitary
73
Lateral area of hypothalamus
Hunger
Destruction --> anorexia, failure to thrive (destruction of lateral hypothalamus makes you shrink laterally)
Stimulated by ghrelin, inhibited by leptin
74
Ventromedial area of hypothalamus
Satiety
Destruction (e.g. craniopharyngioma) --> hyperphagia (if you destroy the ventromedial area of the hypothalamus, it makes you shrink ventrally and medially)
Stimulated by leptin
75
Anterior hypothalamus
Cooling, parasympathetic
Anterior nucleus- Cooling (AC); pArasympathetic- when you rest and digest- you COOL down
76
Posterior hypothalamus
Heating, sympathetic
When you exercise (increase sympathetic response), you back (posterior) gets hot
77
Suprachiasmatic nucleus
Circadian rhythm
You need to sleep to be charismatic (schismatic)
78
Chemoreceptor Trigger Zone
Located within the area postrema of the medulla (floor of the 4th ventricle)
Vomiting control center
Prochlorperazine is an anti-emetic that suppresses dopamine release at the CTZ
79
Sleep physiology
Regulated by the circadian rhythm (suprachiasmatic nucleus)
Controls nocturnal release of ACTH, prolactin, melatonin and NE
80
Path of melatonin release
SCN --> NE release --> pineal gland --> melatonin
Where SCN is regulated by environment (light)
81
Two main stages of sleep
REM and non-REM
Eyes move in REM sleep due to activity of the PPRF (paramedic pontine reticular formation/ conjugate gaze center)
82
REM
occurs every 90 minutes
INCREASED ACh during REM sleep
83
Things that decreases REM sleep
alcohol, benzos, and barbs (also decrease delta wave sleep- Stage N3 of non-REM sleep)
NE (doesn't have effect on N3, but decreases REM)
84
Bedwetting
Tends to occur during N3 Stage of sleep
Tx with desmopressin (rather than imipramine- more SEs)
85
Night terrors, sleep walking
Also occur during N3 stage of sleep
Tx with benzos (decreases N3 stage of sleep)
86
Awake (eyes open)
Alert, active; beta waves (high frequency, low amplitude)
87
Awake (eyes closed)
Alpha waves (lower frequency than beta, low amplitude)
88
Non -REM sleep: N1
Light sleep; Theta waves (hallucinations, hypnogogic)
89
Non-REM sleep: N2
Deeper sleep; sleep spindles and K waves (jaw-clenching/ bruxism)
90
Non-REM sleep: N3
Deepest non-REM sleep; delta waves (low frequency, highest amplitude)
Associated with sleep-walking, night terrors, bed wetting
91
REM sleep
Loss of motor tone, increased brain O2 use, variable pulse and BP
Dreaming, nightmares, and penile/clitoral tumescence
May serve memory processing function
92
Sleep cycle
N1 --> N2 --> N3 --> N2 --> REM --> N1 ...
93
Wave mnemonic: BATS Drink Blood
```
Awake- eyes open (beta)
Awake- eyes closed (alpha)
Sleep- N1 (theta)
Sleep- N2 (sleep spindles & K waves)
Sleep- N3 (delta)
Sleep- REM (beta)
```
94
Thalamus
Major relay for all ascending sensory info (EXCEPT olfaction)
95
Ventral posterolateral (VPL) thalamus
Spinothalamic and DCML --> primary somatosensory cortex
Senses: ST (pain and temp) & DCML (position, touch, vibration, pressure, proprioception)
96
Ventral posteromedial (VML) thalamus
Trigeminal and gustatory --> Primary somatosensory cortex
Senses: Face and taste
97
Lateral geniculate nucleus (LGN)
CN II --> Calacrine sulcus
Senses: vision
98
Medial geniculate nucleus (MGN)
Superior olive and interior colliculus of tectum --> Temporal lobe (auditory cortex)
Senses: Hearing
MGM (MGN) studios has a lot of sounds and music that we HEAR
99
Ventral lateral nucleus (NOT VPL)
Basal ganglia, cerebellum --> Motor cortex
Senses: Motor
100
Limbic system- 5 Fs
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Feeding
Fleeing
Fighting
Feeling
Sex
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Neurons involved in emotion, long-term memory, olfaction, behavior modulation, ANS function
101
Limbic system- components
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Hippocampus
Amygdala
Fornix
Mammillary bodies
Cingulate gyrus
```
102
Dopaminergic pathways- MMNT
Mesocortical (decreased)
Mesolimbic (increased)
Nigrostriatal (decreased)
Tuberoinfundibular (decreased)
()- indicate response that causes altered activity
103
Mesocortical- symptoms of alteration
Decreased activity --> "negative" symptoms (flat affect)
Antipsychotics not very effective; atypical better than typical antipsychotics
104
Mesolimbic- alteration
Increased activity --> "positive" symptoms (delusions, hallucinations)
Main target of antipsychotics (spec. typical)- tx for schizophrenia
105
Nigrostriatal- alteration
Decreased activity- extrapyramidal symptoms (dystonia (involuntary muscle contractions), akathisia (inner restlessness), parkinsonism, tardive dyskinesia)
Significantly affected by movement disorders and antipsychotics (which induce these symptoms)
106
Tuberoinfundibular- alteration
Decreased activity- increased prolactin, decreased libido, sexual dysfunction, galactorrhea, and gynecomastia (in men)
Remember from endocrine: prolactin is inhibited by dopamine and prolactin suppresses GnRH axis
107
Cerebellum- role
Modulates movement; aids in coordination and balance
Somatotopic distrubution
108
Cerebellum- input
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CONTRALATERAL cortex (via middle cerebellar peduncle)
IPSILATERAL proprioception (via inferior cerebellar peduncle/ spinal cord)
```
109
Cerebellum- output
Info sent to CONTRALATERAL motor cortex
| (Purkinje cells --> deep nuclei of cerebellum --> contralateral cortex) via superior cerebellar peduncle
110
Deep nuclei of cerebellum
```
from lateral to medial
Dentate
Emboliform
Globose
Fastigial
```
Emboliform and globose together make the interposed nucleus
111
Lateral lesions
affect VOLUNTARY movement of extremities
| causes IPSILATERAL weakness
112
Medial lesions
involves midline structures (vermal cortex, fastigial nucleus) and flocculonodular lobe (vestibular system)
causes truncal ataxia, nystagmus, head tilting
generally results in bilateral motor deficits (affects axial and proximal limbs)
113
Basal ganglia
Responsible for voluntary movements and postural adjustments
114
Basal ganglia- input
from cortex
115
Basal ganglia- output
back to cortex (negative feedback to modulate movement)
116
Striatum
putamen (motor) and caudate (cognitive)
117
Lentiform
putamen (motor) and globus pallidus
118
Direct pathway
Movement is activated in the presence of dopamine (acts at D1 receptors to facilitate movement)
SN releases DA --> acts at D1 receptors --> stimulates striatum to release GABA --> inhibits GABA release from GPi --> Thalamus becomes disinhibited and movement is allowed
119
Indirect pathway
When dopamine is not present: indirect pathway inhibits movement
Without dopamine acting on D2 receptors --> Striatum stimulated to release GABA --> inhibits GABA release from the GPe --> Causes stimulation of STN (glutaminergic) --> stimulates GABA release from the GPi --> Thalamus is inhibited and movement is halted
120
Effect of Dopamine
Binds to D1 receptors to STIMULATE the excitatory pathway
Binds to D2 receptors to INHIBIT the inhibitory pathway
121
Athetosis
Writhing
Lesion in basal ganglia
122
Chorea
Sudden, jerky movements
Lesion in basal ganglia
123
Dystonia
Involuntary muscle contractions
124
Essential tremor
High frequency tremor with sustained posture
Worsened with movement
Tx: non-selective beta blockers, primidone
125
Hemiballismus
Sudden, flailing arm
Lesion in CONTRALATERAL subthalamic nucleus
126
Intention tremor
Slow, zig-zag motion when pointing/ moving toward target
Sign of cerebellar dysfunction (on ipsilateral side???)
127
Myoclonus
Sudden, brief uncontrolled muscle contraction (e.g. jerks, hiccups)
vs. dystonia (which is sustained contractions)
128
Resting tremor
Uncontrolled movement of distal appendages (e.g. hands)
Gets better with movement
Seen in Parkinson dz (pill-rolling)
129
Parkinson dz symptoms- TRAPS
```
Tremor (resting/ pill-rolling)
Rigidity (cogwheel)
Akinesia (or bradykinesia)
Postural instability
Shuffling gait
```
130
Parkinson dz characteristics
```
Lewi bodies (with alpha-synuclein deposits- eosinophilic inclusions)
Caused by neuron damage and loss of dopaminergic neurons of substantia nigra
```
131
Huntington dz- S&S
choreiform movements, aggression, depression, and dementia (may be mistaken for substance abuse)
Often seen between 20 and 50
132
Huntington dz characteristics
Expansion of CAG repeats- Caudate loses ACh and GABA (C-A-G)
Caused by atrophy of caudate and putamen (striatum)
Increased dopamine, decreased GABA and ACh
Neuronal death caused by NMDA-R binding and glutamate excitotoxicity
133
Sensory vs. motor cortex
Sense BEFORE (somatosensory- posterior) you move (motor- anterior)
134
Broca area
Left inferior frontal lobe (speech)
135
Wernicke area
Left superior temporal lobe (comprehension)
136
Arcuate fasciculus
connection between Broca and Wernicke area
137
Aphasia vs. dysarthria
Aphasia: Higher order language (read/ speak/ write/ understand)
Dysarthria- cannot move vocal cords (motor deficit)
138
Broca Aphasia
Cannot: speak & repeat
Can: understand
139
Wernicke Aphasia
Cannot: Understand & repeat
Can: Speak (doesn't make sense)- but lack insight about their problem
140
Conduction Aphasia
Cannot: Repeat
Can: Speak, Understand
Arcuate fasiculus damage
141
Global Aphasia
Cannot: repeat, speak, or understand
B, W, and AF damaged
142
Transcortical- region near Broca/ Wernicke damaged but some of these regions are spared (repetition is not lost)
Motor (anterior)- near Broca --> cannot speak, but can repeat
Sensory (posterior)- near Wernicke --> cannot understand, but can repeat
Mixed- cannot speak or understand, but can repeat
143
Amygdala lesion
Kluver-Bucy syndrome (disinhibited behavior- hyperphagia, hyper sexuality, hyperorality)
144
Frontal lobe lesion
Disinhibition and concentration & judgement probs
May have reemergence of primitive reflexes
145
Non-dominant parietal cortex lesion
Hemispatial neglect (ignores contralateral side)- more commonly left sided neglect (due to right parietal lobe (non-dominant) injury- because right and left parietal lobe covers right side, but only right parietal lobe covers left side)
In other words, the right parietal lobe covers both sides, and the left parietal lobe covers only the right side --> because it has a lot of other responsibilities (mathematics, writing, etc)
146
Dominant parietal cortex lesion
Agraphia, acalculia, finger agnosia (cannot recognize things), left-right disorientation
147
Reticular activating system (midbrain) lesions
Reduced levels of arousal/ wakefulness
148
Mamillary bodies (bilateral) lesions
Wernicke-Korsakoff (W: confusion, ophthalmoplegia, ataxia vs. K: amnesia (anterograde >> retrograde), confabulation, personality changes)
Associated with B1 (thiamine deficiency) and excess alcohol
149
Wernicke- CAN
Confusion
Ataxia
Nystagmus (ophthalmoplegia)
150
Thiamine deficiency
W-K syndrome/ mammillary body lesions can be precipitated by giving glucose before giving B1 to someone who is deficient
151
Basal ganglia lesions
Tremor at rest, chorea, athetosis (e.g. Parkinson, Huntington)
152
Cerebellar hermisphere lesion
Intention tremor, limb ataxia, loss of balance (limbs- lateral- hemispheres)
Damage to cerebellum --> IPSILATERAL defects (falls toward the side of the lesion)
Can be seen with chronic alcohol use
153
Cerebellar vermis lesion
Truncal ataxia, dysarthria (trunk- central/ midline- vermis)
154
Subthalamic nucleus lesion
CONTRALATERAL hemiballismus
155
Hippocampus (bilateral) lesion
Anterograde amnesia (can't make new memories)
156
Paramedial pontine reticular formation (PPRF) lesion
Eyes look AWAY from side of lesion
157
Frontal eye field lesion
Eyes look TOWARD the side of lesion
158
Homonculus (Medial to lateral)
Feet --> Hands --> Face --> Mouth
More innervation means more representation (e.g. hands, lips, etc.)
159
Cerebral perfusion
Driven by pCO2 (not pO2!!!)
Relies on pressure gradient between MAP and ICP (if MAP is low, or ICP is high --> perfusion (pressure) decreases)
160
Therapeutic hyperventilation
Hyperventilation --> Decreased pCO2 --> Vasoconstriction --> decrease cerebral blood flow and ICP
Used to treat cerebral edema
161
Uncal herniation- classic signs
Single, fixed dilated pupil
162
Classic signs of increased ICP
Coma, bradycardia, HTN (vasoconstriction to decrease ICP), hyperventilation (to decrease ICP), papilledema
163
CPP (cerebral perfusion pressure)
CPP = MAP-ICP if CPP = 0; indicates there is no cerebral perfusion (can cause death)
164
Watershed zones
Between anterior and middle cerebral
Between posterior and middle cerebral
165
Anterior cerebral supplies
Legs (sensory and motor)
Injury causes CONTRALATERAL probs
166
Middle cerebral supplies
Arms and face (sensory and motor)
Broca (frontal) and Wernicke (temporal) area
Injury causes CONTRALATERAL probs + aphasia (if dominant side injured) or hemineglect (if non-dominant side injured)
167
Posterior cerebral supplies
Occipital cortex
Injury causes CONTRALATERAL hemianopia with macular sparing
168
Lenticulostriate artery supplies
Striatum and internal capsule
Injury causes CONTRALATERAL motor and sensory probs to face and body
NO CORTICAL/CORTEX probs- like hemineglect, aphasia, visual field probs- as opposed to middle cerebral infarcts
Associated with lacunar infarcts (unmanaged HTN, smoking)
169
Rule of 12's
Ignore CN 1 and 2...
Medial- if it can divide into 12
Midbrain (3, 4); Pons (6); Medulla (12- tongue deviates ipsilaterally)
Lateral- all others
170
Medial tract syndromes
Medial/ midline- motor syndromes (except for medial lemniscus)
1. Medial lemniscus (vibration/ proprioception)
2. MLF
3. Motor tract of UMN (corticospinal tract)
4. Motor nuclei of CN
171
Lateral tract syndromes
Lateral- sensory syndromes (side)
1. Spinothalamic tract (aka anterolateral, pain and temp); IPSILATERAL face and CONTRALATERAL body
2. Spinocerebellar tract (RAM)
3. Sympathetic chain (Dilation, sweating, etc.); IPSILATERAL to lesion
4. Sensory nuclei of CN
172
Basilar artery
Supplies brainstem
Lesion causes preserved consciousness, vertical eye movement, blinking; quadriplegia, loss of voluntary facial, mouth and tongue movements
173
Aneurysms
Dilation of all layers of an artery due to vessel wall weakening
174
Saccular (berry) aneurysm
Occurs at bifurcation of Circle of Willis (commonly between anterior communicating and anterior cerebral a.)
Causes subarachnoid hemorrhage (worst headache of my life)
175
Berry aneurysm RFs
ADPKD, Ehlers-Danlos, advanced age, HTN, smoking, race (increased in AA), coarctation of aorta
176
Charcot-Bouchard microaneurysm
Associated with HTN
Affects small vessels (e.g. lenticulostriate vessel in basal ganglia and thalamus)
Results in paralysis/ sensory loss of face and body but no cortical/ cortex symptoms (neglect, aphasia, visual field probs)
177
Anterior communicating artery- aneurysm and rupture
Aneurysm/ compression: bitemporal hemianopia (due to compression of optic chiasm)
Rupture: ischemia in ACA (anterior cerebral) distribution- lower limbs motor and sensory probs
178
Posterior communicating artery- aneurysm and rupture
Compression: ipsilateral CN III palsy (mydriasis- dilated/ blown pupil); may also see ptosis (down and out eye)
179
Central post-stroke pain syndrome
Neuropathic pain due to thalamic lesions (10% of stroke patients)
Paresthesias filled by allodynia (pain with normally-painless stimuli)
180
Epidural hematoma- common vessel affected
Middle meningeal a. (branch of maxillary a.)
181
Epidural hematoma- cause
Skull fracture
| vs. pterion fracture also causes middle meningeal a. but not an epidural hematoma because it is lower in the face
182
Epidural hematoma- S&S
Lucid interval, transtentorial herniation CN III palsy
183
Epidural hematoma- CT
Biconvex, does NOT cross suture lines
184
Subdural hematoma- vessel
Bridging veins
185
Subdural hematoma- cause
Acute: trauma
Chronic: alcohol, age, mild trauma, cerebral atrophy
Seen in shaken babies :(
186
Subdural hematoma- CT
Crescent shaped hemorrhage that CROSSES suture lines
187
Subarachnoid hemorrhage- vessel
Aneurysm rupture (e.g. saccular/ berry) or AVM (arteriovenous malformation)
188
Subarachnoid hemorrhage- S&S
"Worst headache of my life"
Bloody or yellow spinal tap
Increased risk of developing communicating and/ or obstructive hydrocephalus
189
Intraparenchymal hemorrhage- vessel
Lenticulostriate vessel (Charcot-Bouchard aneurysm)/ other small vessels
190
Intraparenchymal hemorrhage- cause
Systemic HTN, amyloid angiopathy, vasculitis, neoplasm
191
Ischemia/ stroke- timeline for irreversibility
Begins after 5 minutes of hypoxia
Most vulnerable areas: hippocampus ("HYPOcampus"), neocortex, cerebellum, and watershed areas
192
Stroke- Identification process
IMAGE (non contrast CT) before tPA to ensure that there is no hemorrhage
CT: detects ischemia in 6-24 hrs
Diffusion-weighted MRI: detects ischemia within 3-30 min
193
Histologic features of stroke
```
12-48 hrs: red neurons
24-72 hrs: necrosis and neutrophils
3-5 days: macrophages (microglia)
1-2 wks: reactive gliosis and vascular proliferation
>2 wks: glial scar
```
194
Contraindications for tPA
1. Subarachnoid hemorrhage
2. Uncontrolled HTN > 185 systolic; >110 diastolic
3. AVM
4. Endocarditis
5. Prior surgery (recent)
6. Stroke in past 3 months
195
Ischemic stroke- defn
Blockage of vessel causes disruption of flow and ischemia --> leads to liquefactive necrosis
196
Type of ischemic stroke (3)
1. Thrombotic: clot forms DIRECTLY at site of infarction (most commonly MCA)- usually over atherosclerotic plaque
2. Embolic- embolus from another part of the body obstructs vessel (often affects multiple places and is the result of a-fib, DVT, PFO, etc.)
3. Hypoxic- due to hypoperfusion or hypoxemia (generally affects watershed areas between ACA and MCA & MCA and PCA)
197
Tx for stroke
tPA within 3-4/5 hrs of onset
Reduce recurrence/ risk: medical therapy (e.g. aspirin, clopidogrel); optimum control of BP, blood sugars, lipids, and treat condns that increase risk (e.g. a-fib)
198
Transient ischemic attack
Brief, reversible episode of focal neurologic dysfunction without acute infarction
Generally resolves in <15min
199
TIA-tx
Low dose aspirin to prevent stroke
SE: GI bleeding due to inhibition of COX-1
200
Dura venous sinuses
Large venous sinuses that run through dura and drain blood into internal jugular vein
Also drains CSF from arachnoid granulations
201
Venous sinus thrombosis
presents with signs/ symptoms of increased ICP (headache, seizure, focal neurologic deficits)
can lead to venous hemorrhage
associated with hyper coagulable states (pregnancy, OCP use, Factor V Leiden)
202
Ventricular system pathway
Lateral ventricle --> Interventricular foramen (of Monro) --> 3rd ventricle --> cerebral aqueduct (Sylvian) --> 4th ventricle --> foramens of Luschka (lateral) and Magendie (medial) --> subarachnoid space
203
CSF synthesis
Made by ependymal cells of choroid plexus
Reabsorbed by arachnoid granulations and then drains into dural venous sinuses
204
CSF- purpose
Bathes the brain and spinal cord with nutrients and removes waste products
205
Idiopathic intercranial HTN (aka pseudotumor cerebri)
Increased ICP with no apparent cause via imaging (like hydrocephalus or obstruction)
206
Pseudotumor cerebri RFs
Woman of childbearing age, vitamin A excess, dans, TCNS
207
Pseudotumor cerebri- S&S
headache, diplopia (CN VI palsy) without change in mental status, papilledema
LP: increased opening pressure and headache relief
208
Pseudotumor cerebri- tx
weight loss, acetazolamide, topiramate (anti-epileptic), LPs, CSF shunt placement, optic nerve fenestration surgery
209
Hydrocephalus- defn
increased CSF volume --> ventricular dilation (+/- increased ICP)
210
Communicating hydrocephalus
Decreased CSF absorption by arachnoid granulations
RF: meningitis (inflammation/ scarring)
S&S: increased ICP, papilledema, herniation
211
Normal pressure hydrocephalus
Affects the elderly and is idiopathic
Ventricles expand, but ICP does not increase
S&S: Triad of- urinary incontinence, ataxia, and cognitive dysfunction (wet, wobbly, and wacky) + wide-based/ magnetic gait
212
Non-communicating hydrocephalus
Caused structural blockage of CSF circulation (e.g. stenosis, colloid cyst)
213
Ex vacuo ventriculomegaly
Increased CSF because of tissue/ neuronal atrophy- ICP is normal and triad of symptoms (wet, wobbly, wacky) not seen
214
Nerves-vertebrae relationship
C1-C7 exit above respective vertebrae
C8 exits below C7
All others (T1-S5) exit below respective vertebrae
215
Sinal cord in adulthood
Ends around L1-L2 vertebrae
Subarachnoid space extends to lower border of S2 vertebrae
Lumbar puncture performed at L3-L5 (level of caudal equina to prevent injury to spinal cord); keep spinal cord ALIVE, by puncturing between L3 and L5
216
Tracts- ascending characteristics
SYNAPSE and then cross
217
Dorsal column
Moves up spinal cord IPSILATERALLY, synapses at IPSILATERAL nucleus cuneatus in medulla and then crosses --> continues ascending (now CONTRALATERALLY) in medial lemniscus --> synapses at VPL thalamus --> Sensory cortex (contralateral to sensation)
218
Spinothalamic tract
Enters spinal cord and synapses in gray matter in posterior & ipsilateral spinal cord --> crosses (within this level of spinal cord) at anterior commissure --> ascends up CONTRALATERALLY --> synapses at VPL thalamus --> Sensory cortex (contralateral to sensation)
219
Lateral corticospinal tract
From motor cortex --> travels through internal capsule --> decussates in medulla (pyramids) --> descends CONTRALATERALLY --> synapses at cell bodies in the anterior horn (contralateral to the motor cortex site of signal origin) --> (now LMN) leaves spinal cord and travels to the neuromuscular junction (NMJ)
220
White vs. gray matter
White matter: axons, nerve fibers (on the periphery of the spinal cord)
Gray matter: cell bodies, nuclei, synapses (looks like an H/ butterfly in the spinal cord)
221
+ Romberg sign: decoding
Indicates loss of proprioceptive abilities
DCML origin: if paired with sensory defects
Cerebellar origin: if not paired with sensory defects
222
Motor neuron signs- UMN vs. LMN
Upper: Weakness, Hyperreflexia, Increased tone, Positive Babinski, Spastic paralysis (everything going up)
Lower: Weakness, hyporeflexia, faciculations (muscle twtiching), decreased tone, flaccid paralysis (everything is lowered)
223
Poliomyelitis (asymmetric) and Werdnig-Hoffmann dz (symmetric)
Affects anterior horn (causes LMN lesions)
S&S: LMN lesion- weakness, hypotonia, flaccid paralysis, facciculations, hyporeflexia, muscle atrophy (+ malaise, headache, fever, nausea)
Virus discovered in stool or throat
224
Amyotropic lateral sclerosis
Affects anterior horns and CS tract (UMNs and LMNs are affected)
Tx: riluzole (blocks Na+ channels of damaged neurons)
225
Anterior spinal artery damage
Damages everything (bilaterally) except for the DCML (which are supplied by the posterior spinal arteries)
primarily upper thoracic region (is watershed area), because lower thoracic- below T8- has arterial supply from a. of Adamkiewicz
226
Tabes dorsalis
Damages/ demyelination of DCML
Caused by tertiary (neuro) syphillis (impairs proprioception- causes poor coordination, impairs light touch, impairs vibration)
S&S: + Romberg, DECREASED/ absent DTRs- due to lost sensation?, Argyll pupil (does not react/constrict to light, but can accommodate to objects near and far)
227
Syringomyelia
Causes damage to anterior white commissure (carries fibers of ST/AL tract, therefore bilateral loss of pain and temp sensation in upper extremities)- cape-like distribution
228
Vitamin B12 deficiency
Causes subacute combined degeneration: demyelination of the spinocerebellar tract, corticospinal tract, and DCML
S&S: ataxic gait, paresthesia, and impaired position/ vibration sense
229
Friedrich ataxia- cause
"Ataxic GAAit"
Autosomal recessive
Trinucleotide repeat disorder (GAA)n on chr 9 (encodes frataxin)
GAA repeats frataxin gene impede transcription and therefore reduce translation of this protein
Ataxic GAAit: Causes degeneration of multiple spinal cord tracts
230
Freidrich ataxia- S&S
"Friedrich is Fratastic- he staggers and falls, but has a sweet, big heart"
Staggering gait, frequent falling, nystagmus, dysarthria, hammer toes, high arch (pes cavus), diabetes mellitus, and hypertrophic cardiomyopathy (cause of death)
Presents in childhood as kyphoscoliosis
231
Brown-Sequard syndrome
Hemisection of spinal cord: think of where things cross
Below lesion:
(AL/ ST tract) Pain and temp: contralateral loss
(DCML tract) Light touch, vibration, proprioception: ipsilateral loss
(CS tract) UMN motor symptoms: ipsilateral side of spinal cord damage/ (contralateral motor cortex- because decussates in medulla)
At level of lesion:
LMN signs (hyporeflexia, faciculations, etc.)
Loss of all sensation (AL/ ST and DCML)
232
Frontal lobe damage
Right side- associated with hyper sexuality/ disinhibition
Left side- associated with apathy
