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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
- CO = SV x HR
- BP = CO x TPR
- • 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
- • Decreased BP, decreased 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
- • BP ↑ by 5 – 10 mmHg
- • If standing, Pulse didn’t ↑ by AT LEAST 4 bpm
- • Autonomic Dysfunction
- • Most common cause
- • DM
- • Riley-Day syndrome
- • Shy-Drager
- • Sick Sinus Syndrome
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Riley-Day syndrome
- • Newborn
- • Familial dysautonomia
- • No autonomic reflex
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Shy-Drager syndrome
• Parkinsonian patients that develop autonomic neuropathy
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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
- • patient stands up
- • HR ↑ by > 20
- • BP ↓ below 10 mmHg
- • Carotid massage works by
- • increasing stroke volume to
- • increase firing
- • by CN IX
- • CN X
- • cause reflex bradycardia.
- • Vaso-Vagal Syncope
- • pass out because one induces ↑ reflex bradycardia
- • Hickee
- • Malignant Htn caused
- • cutting CN IX
- • CN IX runs behind the tonsils, so if
- • accidentally cut
- • malignant hypertension.
- • 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
- • going into early shock
- • still compensating
- • Need to hydrate them
- • Will reverse by firing of CN IX, X
- • Check HR 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
- • to Angiotensin I
- • formed in liver
- • Angiotensin I is converted by ACE
- • to Angiotensin II
- • in lungs
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- • Angiotensin II
- • Very potent vasoconstrictor
- • ↑TPR
- • ↑BP
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Ag II - • 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
• Cerebrospinal fluid
• 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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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
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Communicating Hydrocephalus
- • Newborns:
- • mainly premature newborns
- • Intraventricular hemorrhage
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- • Children:
- • due to inflammation
- • Meningitis (posterior fossa)
- • CN 3
- • CN 9
- • CN 10
- • CN 11
- • CN 12
- • Adults:
- • over ingestion of vitamin A
- • Pseudotumor Cerebri
- • Elderly:
- • due to brain atrophy
- • Normal Pressure Hydrocephalus
- • Ventricles enlarg
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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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Noncommunicating Hydrocephalus
• due to an obstruction
- • In newborns:
- • MCC: Aqueductal stenosis
- • 2nd Dandy-Walker cyst
- • In children:
- • meningitis, especially TB
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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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Visual Cortex
• Light must hit the retina by 3 months of age or the child is blind for life
- • You must verify that a child has a RED reflex on eye exam at birth
- • retinal arteries
- • if you can see them
- • nothing is in the way
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Abnormalities of the Eyes: Anisocoria
- • unequal pupil size
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- • MCC: Congenital
- • AD
- • check parents
- • If it occurs in childhood
- • ICP until proven
- • otherwise Dx:
- • CT
- • LP
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Abnormalities of the Eyes: Amblyopia
- • difference in visual acuity
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- • Lazy eye
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- • Tx: Patch the eye up to age 5
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- • Weak muscles
- • CN: 3,4,6
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Abnormalities of the Eyes:
Strabismus
• misalignment of the eyes
- • Esotropia
- • → ←
- • Exotropia
- • ← →
• Weak muscles of the eye
• Tx. Patch good eye
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Abnormalities of the Eyes:
Stigmatism
• corneal defect
- • Straight line card
- • will see a blip in the line
• Convex or a concave defect in the cornea
• Laser keratotomy
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Abnormalities of the Eyes:
My-opia
- • near sightedness
- • can not see far
• Focus of light is before the retina
- • Tx: Concave lens
- • disperses light to sides
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Abnormalities of the Eyes:
Hyperopia
• far sightedness
• Focus of light is behind the retina
- • Tx: Convex lens
- • focuses light earlier in middle
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Abnormalities of the Eyes:
Presbyopia
• loss of accommodation seen with aging
• Due to muscles weakening with age
• Ability to focus on objects coming close
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White Reflex
- • Cataracts
- • opacification of the lens
• Does not allow light to hit the retina
• Must be removed
- • Increased incidence with
- • high glucose or
- • galactose
- • sorbitol or
- • galactitol accumulates
- • Idiopathic: 90%
- • Diabetes or galactosemia
- • Rubella
- • Retinoblastoma
- • Rare
- • Rb gene
- • Cancer
- • High association with Ewing’s sarcoma
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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
- • PCP
- • LSD
- • 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) • 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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Stress Response
- • Parasympathetic discharge
- • always first
- • Sympathetic discharge
- • always second
- • Stress ulcers
- • Curling’s ulcers
- • Cushing’s ulcers
- • triad:
- • bradycardia
- • HTN
- • Increased ICP
- • intracranial pressure
- • IBS
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Subthalamic Nucleus
• Final relay station for coordinating fine motor movements
- • Lesion:
- • Ballismus
- • Hemiballismus
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Substantia Nigra
• Responsible 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
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Parkinson’s Disease Treatment
- • 1st line: L-dopa/ carbidopa
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- • 2nd line: Bromocriptine
- • dopamine agonist
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- • Amantadine
- • Tx influenza A
- • increase DA release from nerve terminal
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- • Selegiline
- • 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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Internal Capsule
• ALL MOTOR fibers going in and out of the brain goes through here
- • Blood supply comes from the lenticulostriate arteries
- • smallest arteries in the brain
- • Lacunar hemorrhages
- • due to HTN
- • Causes significant MOTOR deficits
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Attention Deficit Disorder
• ADD or ADHD (Not focus).
• RAS not working
• Poor Poor attention and focus attention and focus
• Restlessness
• Unable to sit long enough to complete a task
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RAS
• Reticular Activating System
• complex network of neurons located in the brainstem
- • acts as the filter between
- • your senses and
- • conscious awareness
• is naturally dysregulated
- • it under-produces
- • dopamine and
- • norepinephrine
- • struggles to filter out
- • background noise or
- • prioritize important
- • mundane tasks
• makes standard focus feel impossible
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Attention Deficit Disorder Tx
• Central nervous system stimulants
- • methylphenidate
- • 1st in children
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- • Pemoline
- • Dexedrine
- • Adderall
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Mid-Brain
• important functions in motor movement,
- • particularly movements of the
- • eye
- • auditory processing
- • visual processing
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Corticospinal Tract
• CST
• 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 across the frontal cortex
• B-12 deficiency
• ALS
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CST: Increased Intracranial Pressure
- • First sign
- • papilledema
- • optic nerve swelling
- • Second sign
- • esotropia
- • one or both eyes turn inward
- • cross-eyed
- • CN VI paralysis
- • abducens nerve
- • Third sign
- • Sluggish pupils
- • First symptom
- • headache
- • Second symptom
- • diplopia
- • blurred double vision
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CST: If Herniation Continues…
- • Second sign of herniation
- • DECORTICATE posturing
- • involuntary
- • rigid body posture
- • indicating severe brain injury
- • 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
- • superficial muscle
- • long
- • slender
- • 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 anterior white commissure
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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 Damage
- • 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
- • other diseases attack the hemispheres
• Friedreich's ataxia
• Ataxia Telangiectasia
• Adrenoleukodystrophy
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Friedreich's ataxia
• progressive damage to the nervous system
- • retinitis pigmentosa
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- • onset between 10 and 15 years
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- • Initial symptoms may include
- • unsteady posture
- • frequent falling
- • progressive difficulty in walking due to impaired ability to coordinate voluntary movements
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Ataxia Telangiectasia
- • spider vein all over your body
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- • AR
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- • Louis–Bar syndrome
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Adrenoleukodystrophy
- • defective long chain FA
- • Fanconi anemia
- • FA: decreased production of all types of blood cells
• X-linked
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PONS
• Responsible for responding to the environment
- • PNEUMOTACTIC • prevents pneumothorax
- • makes you breath out
- • superior
- • inhibitory to the APNEUSTIC
- • APNEUSTIC
- • makes you breath in
- • bottom
- • responds to
- • pO2 decrease
- • pCO2 increase
• 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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