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Neuro Notes - Exam 1.docx

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Gs Get Degrees
Lesion
Loss of function
Midbrain - Arousal, coordination of chewing , licking, sucking
Crus Cerebri
Loss of motor function of eye- CN III, IV
Superior Colliculi
Motor, sensory and orientation to danger
Inferior colliculi
Hearing loss CN 8 damaged - lateral lemniscus
Posterior cerebral artery(branch of basilar artery)
Superior Cerebellar artery
Posterior communicating artery
Ipsilateral side - CN 3
4
Pons -cardiovascular, breathing control, acoustic, vestibular orientation
Facial colliculus(Caudomedial pontine floor)
Facial muscle, eye muscle problems (CN 6 & 7)
Vestibular Schwannoma- tumor in cerebellopontine angle
CN 7 & 8 function
Basilar artery
Locked in syndrome
Pneumotaxic center
Maintenance of normal breathing pattern
Medulla - expiration, inspiration, vasomotor , swallowing,vomiting
Pyramids
Motor function - weakness
Rostral ventrolateral Medulla (RVLM) - Pressor Area(Glutaminergic)
Loss of control of BP
Caudal Ventrolateral Medulla (CVLM)-Depressor Area(GABAergic)
Decrease in ADH release and inc in BP → Dehydration
Ventromedial Medulla (raphe nuclei)
Dec regulation of temperature,pain, respiration. Lose sympathetic output and constriction of
cutaneous blood vessels.
Nucleus Tractus Solitarius
Hypertension → cardiac damage, pulmonary edema → death
Nucleus Ambiguus
Loss of parasympathetic/visceral response to decrease BP
Dorsal Respiratory group(DRG)
Periodic activation during inspiration, feedback from lung
Gs Get Degrees
Ventral respiratory group(VRG)
Respiratory rhythm generation decreases
control of expiration(dorsal VRG)
inspiration(rostral VRG)
Pre-Botzinger complex in medulla
Respiratory rhythm generator
Phrenic Nucleus
Diaphragmatic contraction
Internal capsule (corticospinal tract) - projection tract
Opposite side motor function is weak
Cerebellum- ​compares motor output with the sensory feedback. Coordinated and steady movement
Cerebellum - Flocculus(CN 8)
Uncoordinated, unsteady movement
Lateral cerebellum
Fine precise control of movements of fingers
Medial cerebellum (vermis)
Up and down movements - control of trunks and limbs
Tonsil herniation
Brain herniates through the foramen magnum
Vermis herniation
Prone to damage medulla
Hypothalamus - integrates endocrine, behavioral info
Posterior Hypothalamus (normal function = Increases body temperature) “it’s
hot in the back”
Decreased body temperature
Hypothermia(decrease in metabolism and motor activity,peripheral vasodilation due to
anterior hypothalamus intact)
Anterior Hypothalamus(normal function = decreases body temperature)
Increased body temperature
Hyperthermia (inc metabolism, shivering, peripheral vasoconstriction -posterior
hypothalamus still intact)
Ventromedial hypothalamus (normal function = inhibits feeding)
obesity
Lateral hypothalamus(normal function = increases feeding)
Decreased feeding (inhibitory neuronal link between arcuate nucleus and lateral
hypothalamus → suppresses food consumption → weight loss)
Pterygoid canal
1.
1.
vasodilation (b/c sympathetics is lost (deep petrosal nerve))
no secretion from nasal, palatine, and lacrimal gland
Gs Get Degrees
2.
loss of general sense and taste sensation of palate (damaged Greater petrosalanterior 2/3 tongue gone)
Brain swelling
Uncus compresses CN III - dilated pupils, sleepiness
Lenticulo striate artery(branch of MCA)
Paralysis of upper body
Intracerebral hemorrhage → obstructive hydrocephalus(Inc ICP)
Corticobulbar tract
Loss of motor function of CN
Suprasacral spinal transection(Above T12)
Automatic bladder- bladder is filled until a threshold is reached → reflexing emptying
Midsacral afferents (cauda equina)
Atonic bladder → loss of afferents - bladder is filled and leads to urinary retention due to
loss of reflexive arc(micturition center) → urine dribbling
Lateral brain- MCA dominant
Language deficit(understanding decreases-Wernicke’s and- Broca’s), weak mouth and face
Medial brain- ACA dominant in anteromedial
PCA is posteromedial
ACA- left Leg, foot weakness, loss of voluntary control of bowel and bladder (incontinence)
PCA - CN3 - Central vision is preserved but cannot see periphery, amnesia
Anterior spinal artery (ventral 2/3rd of spinal cord) - somatosensation
(Lateral column)
Cannot tell pain and temperature(ASA)
Paralysis(lateral column)
Posterior spinal artery
Dorsal column of the ipsilateral side
Herpes
Temporal lobe
Prolactinoma -pituitary gland tumor
Compresses optic chiasm - Decrease in endocrine cells,Optic nerve dysfunction
Fornix (connects hippocampus to mamillary body)
Amnesia, Korsakoff
Dorsal-column medial lemniscal system
Detect position, vibration
Spinothalamic tract
Pain and temperature
Corticospinal(cortical layer V)
Voluntary movement -strength decreases
Circumventricular organs - Subfornical organs, organum vasculosum lamina
terminalis
Decreased secretion of ADH, decreased control of regulation of electrolytes
Amygdala
Decreased emotion and fear response
No response to olfactory stimulus
Gs Get Degrees
Solitary Nucleus
Decreased response to pain,temperature and special afferents(taste) from CN 7,9,10
Anterior Paracentral
Weakness in contralateral lower extremity
Mastoiditis
Petrous part of temporal bone
Inferior frontal gyrus(pars operacularis and triangularis)
Lose Broca’s speech area
Lateral funiculus
Weakness in arm and leg
Middle meningioma
Parieto-occipital sulcus
Forebrain Autonomic control● Circumventricular organs ​- Subfornical organ , organum vasculosum of lamina terminalis
Lack BBB
Detect electrolyte changes - project to hypothalamus e.g. Regulate ADH secretion
●
Insular cortex​: Receives visceral pain, temperature, taste sensations via thalamus and integrate with emotion
●
Anterior cingulate cortex:​ anterior portion of the limbic lobe. Controls autonomic output via connections with insula, prefrontal cortex, amygdala,
hypothalamus & brainstem.
●
-
Amygdala​ - regulates stress and fear response.
Receives direct input from ​olfactory system​ & other solitary nucleus
Output fibers to hypothalamus via stria terminalis & to brainstem including periaqueductal grey & reticular formation
●
Hypothalamus : integrates autonomic, endocrine, motivated behavior. Basic life processes - BP, body temp, energy metabolism, reproduction, emergency
response
Hypothalamic control of anterior pituitary
Parvocellular neuroendocrine cells within Paraventricular, arcuate nucleus → terminate in primary capillary plexus of superior hypophyseal artery of the
infundibulum(pituitary stalk).
Pathway is called tubero-infundibular tract
Primary capillary plexus → neuroendocrine substances enter blood, neurohormones of post pituitary act on non endocrine cells. ---> portal veins → anterior
pituitary → secondary capillary plexus
Gs Get Degrees
● Feeding behavior regulated by hypothalamus
Ventromedial nucleus ​of medial hypothalamus - suppresses feeding
Lateral hypothalamus ​- promotes feeding(inhibited by leptin release from adipose tissue)
●
-
Regulation of body temp
Anterior hypothalamus ​: dec body temp(integrate autonomic control - dilation of skin arterioles, sweating; motivated behavior-seeking cooler
environment, remove clothing)
Posterior​ : inc body temp(constriction of skin arterioles; motivated behavior-shivering,seeking warmer environment, add clothing)
Autonomics Lecture 20
●
Bladder control : ​CNS at supratentorial level, posterior fossa and spinal cord
Gs Get Degrees
Lecture 21 : Neurons and Glia
●
●
●
●
Primary sensory afferents : pseudounipolar
Central or peripheral special sensory : bipolar
Long axons(golgi type 1) e.g. motor neurons, short axons(golgi type II) e.g. local interneurons - multipolar
●
-
Radial Gli​a - neuronal, astrocytic, oligodendrocyte progenitors. Scaffold for neuronal migration
Become bergmann glia in cerebellum
Become muller cells of the retina
● Astrocytes: ​Regulate Ions
Synaptic transmitters
Regional cerebral blood flow
Neuroprotection:
BBB
Limit oxidative damage
Supply lactate
Release gliotransmitter
Form gliotic scars
● Microglia:​ immunocompetent and phagocytic - protect neurons from micro-organisms and toxic effects of cellular debris.
Secrete neurotrophic or neuron survival factors upon activation
Release cytotoxic molecules : pro-inflammatory cytokines, reactive oxygen intermediates, proteases
Contribute to pathological neuronal degeneration
Gs Get Degrees
-
Tanycytes: ​derived from radial glia. Functional interface between blood and CSF around 3rd ventricle
Present near circumventricular organs. Also secrete CSF and transport of hormones
Blood Supply: ​Circle of WIllis - surrounds optic chiasm,optic tract, mammillary body, ventral
hypothalamus - anastomosis at diencephalon
Circle of Willis is formed by proximal branches of posterior cere- bral artery, posterior
communicating arteries, a part of internal carotid artery prior to its bifurcation,
proximal part of anterior cerebral artery, and anterior communicating arteries
Brachiocep​halic trunk→ right common carotid
Aortic arch → left common carotid
Common carotid​ → internal and external division at the thyroid
I​nternal carotid artery​→ ophthalmic, anterior choroidal, p
​ osterior communicating artery branches
→ ​middle cerebral artery (​terminal branch of ICA) : runs laterally over insula & supplies temporal &
parietal lobes(Wernicke’s, Broca’s) → L
​ enticulo striate artery​ supplies basal ganglia, internal
capsule(rupture=intracerebral hemorrhage)
→A
​ nterior cerebral artery​ (terminal branch of ICA):runs medial to optic chiasm and supplies frontal
Anterior communicating​ artery(common spot for aneurysm) supplies frontal, parietal lobes, septum pellucidum, corpus callosum
lobe.
Subclavian artery → Vertebral artery →
​ ​Posterior inferior cerebellar arteries(PICA)​ & ​Anterior spinal artery (ASA)​ supplies pyramids, ​PSA​(supplies dorsal column)
→ combine to form B
​ asilar artery ​→ A
​ nterior inferior cerebellar artery(​AICA)(CN 6,7&8) , ​Labyrinthine artery, Pontine, superior cerebellar, posterior cerebral(​pons
and midbrain junction)
Midbrain:
1. Posterior cerebral artery
2. Superior cerebellar artery
3. Posterior communicating artery
Pons : Long and short circumferential, paramedian branches of basilar artery
Medulla :
1. Posterior inferior cerebellar
2. Anterior inferior cerebellar(CN 7&8),
3. ASA (medial area)
●
●
Interhemispheric : Corpus callosum Intrahemispheric : association e.g arcuate fasciculus
Gs Get Degrees
Lecture 24:
● Hyperosmolality weakens BBB but its reversible so it can permit the delivery of lipid-insoluble drugs to the CNS
●
●
●
-
Sensory receptors express receptor potential
Other neurons express postsynaptic potentials
Greater length constant → lesser decrement. (increase in diameter)
Lower intracellular resistance
Greater membrane resistance
●
-
Initiation zone: populated by voltage gated sodium channels
Multipolar: IZ is at the axon hillock and origin of graded potential: dendrites
bipolar : IZ and graded receptor potential at the presynaptic terminal
●
●
Compared to plasma - CSF has high Cl- , Mg2+ and high to normal Na+
Lumbar Puncture for adults : L3/L4. For children L4/L5. Measure CSF pressure - normal 65-200mm H2O (<15mmHg)
●
Glucose and L-DOPA cross BBB through facilitated diffusion but dopamine weakly accesses the brain
●
a)
b)
c)
d)
e)
f)
g)
Factors that weaken BBB:
Hypertension
Hyperosmolarity : may permit delivery of lipid-insoluble drugs to the CNS
Trauma
Ischemia
Inflammation
Pressure
infection
Gs Get Degrees
●
Sensory neurons- IZ is close to sensory ending
Lidocaine: block voltage gated Na+ channels - disrupts AP (not graded potentials) → treat pain
Botulinum toxin : blocks Ach release. ​Binds to cholinergic nerve endings after ingestion → enters the cell via retrograde transport(dynein driven) → suppresses
docking by cleaving synaptobrevin → prevents vesicular release of ACH ​irreversibly ​→ weakness!!
Tetanus toxin : ​enters PNS via wound → retrograde transport → enters ​gkycinergic interneurons​ → suppresses docking by cleaving synaptobrevin →
irreversible suppression of glycine release → disinhibits LMN → m
​ uscular spasm “​opisthotonus”
Aminoglycoside antibiotics: Neomycin inhibits exocytosis Ach at motor nerve terminals ​→ block presynaptic calcium channels. Effects of both antibiotics
are reversed by elevated extracellular Ca2+
Gs Get Degrees
4-Aminopyridine : ​K+ channel blocking drug prolongs duration of the impulse → enhances Ca2+ entry into motor nerve endings → Inc AcH release → Inc
quantum content
GABAa binding agonist
Benzodiazepines
Barbiturates
Neurotransmitter
Achetylcholine
Nuclei ( → projects into)
1)
2)
Glutamate
Receptor
Basal forebrain: Basal nucleus of Meynert → cortex, limbic
system -​ involved with Alzheimer's
Dorsolateral pontine tegmental → brainstem, thalamus,
hypothalamus, basal ganglia, cerebellum : motor control of
movement
Ubiquitous (everywhere)
GABA
1)
2)
-
Small GABAergic neurons are ubiquitous modulators
Longer GABAergic pathways arise from varied nuclei
Striatum → substantia nigra
Substantia nigra → superior colliculus and thalamus
Medial vestibular nuclei → spinal cord
Cerebellar cortex → deep cerebellar nuclei
Glycine
-
Neurons are small local regulators
Found near spinal and bulbar motor nuclei
a)
AMPA/Quisqualate kainate : ionotropic
cationic : Na+ influx, K+ efflux
b) NMDA : glutamate binds, glycine has to
occupy the strychnine-insensitive binding
sites
Non-NMDA receptor mediated
depolarization - Mg2+ removed → Na+,
Ca2+ influx and K+ efflux
Aspartate uses same receptor
GABAa - ionotropic - Cl- passing receptor
> benzodiazepines works with GABA(a) to allow Cl> barbiturates can work independently
GABAb - metabotropic: inc K+ efflux and
Ca2+ dec influx → axoaxonic → reduce
NT release
-
Dopamine
1.
2.
Substantia nigra pars compacta → via nigrostriatal pathway →
caudate and putamen (motor function) - ​Parkinson's affects
midbrain
Ventral tegmental area situated medial to substantia nigra
Structurally and functionally similar to
GABAa receptors - Cl- conducting
(ionotropic)
Blocked by strychnine
Metabotropic : D1 like (D1 & D5): excitatory
coupled to cAMP
D2 like (D2, D3, D4) - inhibitory coupling to cAMP
Gs Get Degrees
-
Prefrontal cortex (mesocortical pathway) - increase schizophrenia
Nucleus accumbens and limbic structures(mesolimbic pathway) happy center
3. Hypothalamic arcuate nucleus → hypothalamic median eminence
for dumping of DA into hypophyseal portal system → inhibits prolactin
Norepinephrine
1.
2.
Serotonin
(Nuclei- only one found in
brainstem)
Locus coeruleus → diencephalon, limbic system, cerebral lobes
and cerebellum​ ( indicated in depression)
Other clusters of pontomedullary noradrenergic nuclei project →
NTS and spinal targets
Array of midline brainstem(raphe)
Mesencephalic and pontine nuclei → thalamus , limbic areas,
cortex (Depression)
Medullary serotonergic cells → within the medulla and to spinal
cord
Metabotropic : a1 and B1 excitatory
a2 & b2 inhibitory
Metabotropic
5-Ht1, 5-Ht5 : inhibitory
5-Ht2: excitatory
5-HT3: excitatory ionotropic (cation -permeable)
5-HT4, 5-HT6, 5-HT7 : excitatory
Rheumatic fever case:
Age: young children ~ 6 year olds
No milestone delays, development is normal. Everything else is NORMAL.
Sensory:​ & neural examination : normal
Deep tendon reflexes : normal’
MRI : normal
Symptom: unusual hyperactivity, involuntary movement (hyperkinesia) → getting worse, tongue protrusion, recurrent sore throat, enlarged tonsils
Acute Rheumatic fever - Carditis, arthritis major things found.
Lesion? - BASAL GANGLIA
What constitutes it? - Caudate Nuceus, Putamen, Globus pallidus
Gs Get Degrees
Sydenham Chorea
MRI: abnormal
Inflammation
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