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Fxn of the brain
• The brain is sensitive to changes in pCO2
• The periphery is sensitive to HYPOXIA (pO2 ↓)
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Carotid Bodies
• Control immediate changes in BP
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Carotid sinus
• Baroreceptor that regulates BP
• SENSES stroke volume (SV) → via response to stretch
• CN IX & X are always firing
- • Anything that drops SV (standing for a long time)
- • Will decrease firing by CN IX and X
- • Will increase HR (reflex tachycardia) and increase BP
- • Reflex Tachycardia occurs because sympathetic innervation is no longer opposed and DOMINATES → ↑ BP
- • β1 Blocker will ↓ HR by inhibiting Reflex Tachy.
• Anything that will increase stroke volume
• Will increase firing by CN IX and X
• Therefore, decrease BP and decrease HR =
- • Reflex Bradycardia
- • When stand up
- • BP drops 5-10mm Hg
- • Pulse 5-10 bpm
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Carotid sinus (Autonomic neuropathy)
• When standing up the HR ↑ by 5-10 bpm and BP ↑ by 5 – 10 mmHg
• But Pulse didn’t by AT LEAST 4 bpm = Autonomic Dysfunction
- • Most common cause = DM
- • Riley-Day syndrome = Newborn
- • Familial dysautonomia
- • No autonomic reflex
- • Shy-Drager
- • patients that develop autonomic neuropathy
- • Sick Sinus Syndrome → Elderly
- • Calcification of the carotid sinus due to aging
- • Old lady will pass out when standing up
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Carotid sinus (other fxns)
• If the BP decreased by > 10 mmHg there is more going on than a reflex problem
- • Orthostatic Hypotension
- • HR ↑ by > 20 or if the BP ↓ below 10 mmHg when the patient stands up
• Carotid massage works by increasing stroke volume to increase firing by CN IX and X and cause reflex bradycardia.
•Vaso-Vagal Syncope → pass out because one induces ↑ reflex bradycardia
• Hickee
• Malignant Htn. caused by cutting CN IX
• CN IX runs behind the tonsils, so if accidentally cut will create malignant hypertension. Will cause reflex tachycardia.
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Intermediate Control of BP
• If reflex tachycardia is not enough NE will come out as 2nd messenger
- • High affinity for a receptor
- • Then affinity for b receptor
- • Increasing HR by a lot (NE & HR ↑ together)
- • TPR goes up every time Stroke volume is low.
- • Normal BP and High HR means going into early shock, still compensating.
- • Need to hydrate them
- • Will reverse by firing of CN IX & X
- • Check HR to monitor for adequate hydration
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Long term Control of BP
• Stimulate JG apparatus- by low flow to the kidneys.
- • Renin comes out
- • Cuts Angiotensinogen (formed in liver) to Angiotensin I
- • Angiotensin I is converted by ACE (in lungs) to Angiotensin II
- • Angiotensin II
- • Very potent vasoconstrictor
- • ↑TPR
- • ↑BP
- • Ag II will also stimulates Aldosterone
- • To decrease loss of volume
- • Aldosterone goes to kidney and reabsorbs Na from DCT
- • Excretes K in the process.
- • Serum Na will be diluted and decreased. Because Na brings in 3x the Water!!!
- • Serum Cl will also decrease due to dilution
- • Serum K will decrease because of secretion
- • Also excretes H+
- • Serum pH will go up
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CSF
• A filtrate of plasma
• To add cushion for the brain
• Made by the Choroid Plexus in each ventricle
• Requires Vitamin A
• Requires Carbonic Anhydrase
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How CSF differs from plasma
• Less HCO3-
• More CL-
• Lower pH 7.34 (acidic)
• Up to 25 WBCs normal in first month of life normal
• >1 month, only up to 3 WBCs normal
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LOW VOLUME STATE (after chronic period of time)
Will always present with:
- • Hypertension
- • ↑TPR → Renin/Angio System
- • ↑BP
- • ↓Na → Aldosterone
- • ↓K → Aldosterone
- • ↑pH (metabolic alkalosis)
- • Examples:
- • CHF
- • Pregnant woman with emesis
- • Child with projectile vomiting
- • Patient with renal artery stenosis
- • Exercise
- • ANY TIME ↓ Blood flow to the kidneys!!!
3 Exceptions: Low volume states that present with METABOLIC ACIDOSIS
- 1. Diarrhea → loss of HCO3-
- 2. DKA → ↑ ketones
- 3. RTA II – loss of HCO3-
GOES ON TO THE LOW ENERGY STATE
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Vomiting Centers
• Chemotactic Trigger Zone: located on the floor of the 4th ventricle
- • Responds to any increase in ICP
- • Stimulated by dopamine
• Area Postrema: located on the blood side of the blood brain barrier (BBB)
- • Responds to offensive smells or taste
- • Stimulated by dopamine
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Hydrocephalus
• Non-communicating:
• due to an obstruction
- • Communicating:
- • overproduction of CSF
- • Newborns: mainly premature newborns
- • Intraventricular hemorrhage
- • Children: due to inflammation
- • Meningitis (posterior fossa) CN 3,
- 9,10,11,12
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Noncommunicating Hydrocephalus
• due to an obstruction
• In newborns:
- • MCC: Aqueductal stenosis
- • 2nd Dandy-Walker cyst
• In children: meningitis, especially TB
• In adults: cancer
• In elderly: cancer
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Communicating Hydrocephalus
• overproduction of CSF
• Newborns: mainly premature newborns
• Intraventricular hemorrhage
• Children: due to inflammation
• Meningitis (posterior fossa) CN 3, 9,10,11,12
• Adults: over ingestion of vitamin A
• Pseudotumor Cerebri
• Elderly: due to brain atrophy
- • Normal Pressure Hydrocephalus
- • Ventricles enlarge
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Normal Pressure Hydrocephalus
• Ventricles expands as the brain atrophies
• Enlarged ventricles then compress the long midline fibers that go to the bladder and legs
• Triad:
- • Dementia
- • Incontinence
- • Ataxia (degenerative disease of the nervous system)
• Tx: VP shunt
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Sturge Weber Syndrome
• Benign port wine stain- capillaries
• Opthalmic branch of CN V
• Mental retardation
• Seizure
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Osler-Weber Rendu Syndrome
• Small aneurysmal telangiectasia on the skin and mucus membrane
• Causes GI bleeding
• Pulmonary AV fistula
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Tuberous sclerosis: benign tumors
• AD
• Mental retardation
• Seizure
• Retinal angiomyolipoma
• Cardiac rhabdomyoma
• Pancreatic cyst / Coloboma
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Von-Hippel Lindau
• Cerebellar hemangioma
• Retinal hemangioma
• Renal cell carcinoma (increased EPO’s)
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Frontal Lobe
• CST (corticospinal tract) motor fibers originates from here
• Unique information:
- • Personality – is stored in the frontal lobe
- • Abstract reasoning
- • (don’t cry over spilled milk)
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Frontal Lobe Lesions
• Atonic seizures- generalized (knock out CST)
• Dementias
- • Alzheimer's
- • Pick’s disease
• Schizophrenia: loss of asymmetry
• Frontal lobotomies
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Temporal Lobe
• Hearing
• Balance
• Hallucinations ( released by serotonin)
• Posterior temporal lobe: Wernicke’s area
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Parietal Lobes
• Dominant lobe: long term memory; all the things you learned since kindergarten
• left side is dominant in 90% of right-handed and left-handed people
• Nondominant lobe: apraxia (motor disorder) and hemineglect (patients fail to be aware of items to one side of space)
• Right side is nondominant in 90% of righthanded and left-handed people
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Epidural Hematoma
• Middle meningeal artery
• Fracture of temporal bone
• Lucid interval
• temporary improvement in a patient's condition after a traumatic brain injury, after which the condition deteriorates
• Lenticular shape
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Subdural Hematoma
• Bridging vein
• Venous bleed
• Delayed onset
• Shaken baby
• Elderly
• Crescent shape
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Subarachnoid Hemorrhage
• Aneurysm rupture
• Worst headache of their life
• Bloody spinal tap
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Epithalamus
• The ONLY nucleus with NO known function
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Thalamus
• ALL SENSORY information in and out of the brain MUST stop here
• ALL information about the ARMS stay LATERAL
• ALL information about the LEGS stay MEDIAL
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Hypothalamus
• Controls hunger
- • Hunger center: lateral
- • Satiety center: medial- 80% NE and 5HT (+)
- • You can override via cortex – stimulus “FOOD”
• Controls menstrual cycle
• Controls temperature
- • Anterior: cools
- • Posterior: warms
• Controls stress response (NE release)
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Subthalamic Nucleus
• Final relay station for coordinating fine motor movements
• Lesion: Ballismus and Hemiballismus
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Substantia Nigra
• Responsible for INITIATING movements
• Uses DOPAMINE for neurotransmitter
• Receives inhibitory signals from basal ganglia via ACH or GABA
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Parkinson’s Disease
• Loss of DOPAMINE fibers from substantia nigra to striatum (caudate and putamen)
- • Unable to initiate activities
- • Mask like facies
- • Bradykinesia
- • Shuffling gait
- • Pill rolling tremor
- • Autonomic dysfunction: Shy Dragger syndrome
• Treatment: L-dopa/ carbidopa
- • 2nd line: Bromocryptine (dopamine agonist)
- • Amantadine (Tx influenza A)- increase DA
- release from nerve terminal
- • Selegyline (MAO-B inhibitor)- prevent DA
- breakdown
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Huntington’s disease (Movement disorder)
- • 90%
- • AD
- • Trinucleotide repeats
- • Caudate nucleus involved
- • Anticipation
- • Decreased GABA fibers
- • Treat with DA blockers (they have too much DA)
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Wilson’s disease (Movement disorder)
- • < 10%
- • AR
- • Ceruloplasmin def
- • Copper excess
- • Lenticular nucleus involved
- • Kayser-Fleischer rings
- • Liver involvement
- • Treat with penicillamine
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Attention Deficit Disorder
• Tx:
- • methylphenidate (1st in children);
- • pemoline; dexadrine; adderal
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Mid-Brain
important functions in motor movement, particularly movements of the eye, and in auditory and visual processing
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Corticospinal Tract
• Responsible for fine motor activity
• Has to inhibit extension so that smooth flexion can occur
• Fibers originate from the frontal lobes, the precentral gyri
• Fibers descend through the internal capsule and CROSS at the medullary pyramids
•Spasticity- can not flex
•Babinski – extension of toes
•Hyperreflexia
•Clonus
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CST Pathology
• Atonic seizures: depolarization goes across the frontal cortex
• B-12 deficiency
• ALS
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CST: Increased Intracranial Pressure
• First sign: papilledema (optic nerve)
• First symptom: headache
• Second sign: esotropia (CN VI paralysis) abdusence
• Second symptom: diplopia or blurred vision
• Third sign: Sluggish pupils
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CST: If Herniation Continues…
• Second sign of herniation: DECORTICATE posturing
• Compression has occurred below CN III but above the red nucleus
• Red nucleus still makes the upper extremities flex while the legs extend
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CST: Final Ending
• Herniation goes beyond the red nucleus
• CST and Corticorubral and rubrospinal tracts are all lost
• All extremities will extend by default
• Medulla is pushed through the foramen magnum.
• DECEREBRATE posturing
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Dorsal Columns
• Gracilis: carries leg fibers; located MEDIALLY
- • S = sacral
- • L = lumbar
- • T = thoracic
• Cuneatus: carries arm fibers; located LATTERLY
• C = cervical
• Vibratory sensation
• Two-point discrimination
• Position sense
• (toe movement)
• Conscious proprioception
• (eyes closed knowing what he is doing)
• The only sensory pathway with four synapses
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Dorsal Columns (Synapse)
• FIRST SYNAPSE: dorsal root ganglion
- • Fasciculus gracilis: ( lower extremities)
- • Fasciculus cuneatus: ( upper extremities)
• SECOND SYNAPSE: MEDULLA
• THIRD SYNAPSE: THALAMUS
• FOURTH SYNAPSE: parietal lobes
• ( postcentral gyri)- ALL SENSORY
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Dorsal Column Pathology
- • Syphilis
- • Vitamin B-12 Def
- • Brown-Sequard
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Spinothalamic Tract
• Pain and Temperature
• (opposite all other lesions)
•The only pathway that CROSSES in the spinal cord (only one)
•Fibers enter the spinal cord, ascend two levels, then cross to opposite side via the anterior white commisure
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Spinothalamic Tract (Synapse)
• FIRST SYNAPSE: dorsal root ganglion
• SECOND SYNAPSE: thalamus
•THIRD SYNAPSE: parietal lobes
• ( postcentral gyri)- Sensory
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Spinocerebellar Pathway
• The only pathway in the spinal cord that crosses twice ( equivalent to ipsilateral)
•Responsible for depth perception
• Signs of damage:
- • INTENTION TREMOR (during reach)
- • DYSMETRIA (heal to shin) or PRONATOR DRIFT
- • DYSDIODOKINESIS (rapid movement)
- • ROMBERG SIGN (loss of unconscious proprioception)
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Spinocerebellar Pathway
• This pathway does NOT reach the cortex
• Unconscious proprioception
• (don’t have to think about it)
• FIRST SYNAPSE: dorsal root ganglion
• SECOND SYNAPSE: thalamus
• THIRD SYNAPSE: cerebellum
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Spinocerebellar Pathway Pathology
• Alcohol attacks the vermis (midline) of the cerebellum while other diseases attack the hemispheres
• Fredrieck’s Ataxia-retinitis pigmentosa
• onset between 10 and 15 years. Initial symptoms may include unsteady posture, frequent falling, and progressive difficulty in walking due to impaired ability to coordinate voluntary movements
• Ataxia Telangiectasia- spider vein all over your body
• Adrenoleukodystrophy- defective long chain FA (Fanconi anemia)
- • X-linked
- • FA: decreased production of all types of blood cells
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PONS
• Responsible for responding to the environment
• Contains the
• PNEUMOTACTIC (superior)inhibitory to the APNEUSTIC (bottom) responds to pO2 dec., pCO2 inc.
• CNS area most sensitive to osmotic shifts
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Pons – Pathology
• Locked-in Syndrome
• Central Pontine Demyelinolysis
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Medulla
• Controls ALL basic functions
• Respiration of 8-10 ipm
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