Neuro Flashcards
Which cells hypertrophy and scar in response to CNS injury?
Astrocytes
Which cells regulate CNS blood flow by contacting CNS capillaries?
Astrocytes
Which cells form an “immune system” within the CNS?
Microglia - phagocytose dead cells
o The microglia at the repair stage after ischemia have a high lipid content because of the extensive phagocytosis of myelin breakdown products
CN 1
Olfactory
Smell
(Sensory)
Exits via cribiform plate
CN 2
Optic
Sight
(Sensory)
Exits via optic canal
CN 3
Oculomotor
Eye movement, pupillary constriction, accomodation, eyelid opening
(Motor)
Exits via superior orbital fissure
CN 4
Trochlear
Depression and inward eye movement: superior oblique muscle
(Motor)
Exits via superior orbital fissure
CN 5
Trigeminal
Mastication, facial sensation (V1, V2, V3), sensation of anterior 2/3 of tongue, tensor tympani muscle
(Both: motor and sensory)
V1: superior orbital fissure
V2: foramen rotundum
V3: foramen ovale
CN 6
Abducens
Outward eye movements: Lacteral rectus muscle
(Motor)
Exits via superior orbital fissure
CN 7
Facial
Facial expression, taste of anterior 2/3 of tongue, lacrimation, salivation, eye lid closing (orbicularis oculi), stapedius muscle
(Both: motor and sensory)
Exits via internal acoustic meatus
CN 8
Vestibulococular
Hearing, balance
(Sensory)
Exits via internal acoustic meatus
CN 9
Glossopharyngeal
Taste and somatosensation of post 1/3 of tongue, swallowing, salivation from parotid gland, stylopharyngeus muscle
(Both: motor and sensory)
Exits via jugular foramen
CN 10
Vagus
Taste from epiglottis, soft palate elevation, talking, coughing, thoracic and abdominal viscera autonomics
(Both: motor and sensory)
Exits via jugular foramen
CN 11
Accessory
Head turning, shoulder shrugging (sternocleidomastoid and trapezius muscles)
(Motor)
Exits via jugular foramen
CN 12
Hypoglossal
Tongue movement
(Motor)
Exits via hypoglossal canal
Charcot-Marie-Tooth Disease
Mutations in connexin 32 protein leads to nonfunctional gap junctions (demyelination) → slow but progressive loss of motor and sensory activity
Epidural Bleed
Tearing of the middle meningeal artery secondary to temporal bone trauma
Localized
Lens shaped
Does not cross suture lines
Subdural bleed
Tearing of the bridging veins as they enter dural venous sinuses
Large
Crescent shaped
Crosses suture lines
Seen in alcoholics, elderly, and shaken babies
Subarachnoid bleed: caused by what and what is an important sequela to take under consideratin
Secondary to rupture of ordinary arteries and veins (berry aneurysm), fills sulci and cisterns
Bleeding between the arachnoid mater and pia mater
Berry aneurysms are associated with EDS and ADPKD
4-10 days after hemorrhage, vasospasm can occur and cause an ischemic infarct (prevent this with Nimodipine – dihydropyradine Calcium channel blocker)
What do Golgi tendon organs detect? What do muscle spindles detect?
Golgi - detect Force generated in muscle (has nothing to do with stretch) – In passive movements, golgi tendon organs are not activated
muscle spindles detect stretch
Gemistocytic astrocytes
Astrocytes turn into these in response to a pathologic process.
Lay down glial fibers.
Multiple Sclerosis
S/S
Hypersensitivity?
Autoimmune inflammation and demyelination in the CNS (destruction of oligodendrocytes)
Type IV hypersensitivity
SIN: Scanning speech, Intention tremor/Incontinence/Internuclear opthalmoplegia, Nystagmus
Relapsing and remitting course with gradual downhill progression
See plaques of demyelination in periventricular white matter
CSF findings in Multiple Sclerosis
Increased immunoglobulins with oligoclonal IgG bands and myelin basic protein
Internuclear opthalmoplagia
Seen in MS
A lesion in the medial longitudinal fasciculus of the brain stem
if right MLF is affected – when the patient looks left and the left CN6 fires to contract the lateral rectus muscle, the lack of communication to Right CN 3 (via defective MLF) will cause the right eye to lag behind due to lack of contraction of the medial rectus muscle
Central pontine myelinosis
Massive axonal demyelination in pontine white matter secondary to osmotic changes (alcoholism, electrolyte imbalance, rapid correction of hyponatremia)
Rapid onset of paralysis, dysarthria, loss of consciousness, locked in syndrome
Correcting serum Na levels too fast
“From high to low your brain will blow” Cerebral edema/herniation
“From low to high your pons with die” Central pontine myelinosis
Guillain Barre Syndrome
Autoimmune condition (likely due to molecular mimicry) that causes destruction of Schwann cells in the PNS Histo: Endoneural inflammatory infiltration with multifocal demyelination
Ascending paralysis that can affect the respiratory muscles
Associated with Campylobacter jejuni or Influenza infection
Sturge-Weber Syndrome
affects small blood vessels (port wine stain), ipsilateral leptomeningeal angioma, seizures, eoiscleral hemangioma → inc intraocular pressure leading to early onset glaucoma
Where does anterior brain blood supply come from?
Internal carotids –> MCA and ACA
Where does posterior brain blood supply come from?
Vertebral arteries –> Basilar a –> PCA
Patient presents with right arm and face paralysis and loss of sensation to the same areas. where is the infarct?
Left middle cerebral artery (MCA)
Patient presents with left leg weakness and loss of sensation, where is the infarct?
Right anterior cerebral artery (ACA)
Patient presents with visual deficits, where is the infarct?
Posterior cerebral artery (PCA)
Stroke in which artery causes “locked in syndrome?”
Basilar artery
Supplies the pons, medulla, lower midbrain, corticospinal and corticobulbar tracts
Progression of stroke histology
1) red neurons (red = dead) - 12 hours
2) Neutrophils - 1 day
3) Macrophages/microglia (days)
4) reactive gliosis and vascular proliferation (1 week) liquefactive necrosis
5) Glial scar (>2 weeks)
Midbrain nuclei
Pontine nuclei
Medulla nuclei
Spinal cord nuclei
Midbrain nuclei: CN 3 and 4
Pontine nuclei: CN 5, 6, 7, 8
Medulla nuclei: CN 9, 10, 12
Spinal cord nuclei: CN 11
Cause of subacute pancencephalitis
Persistent infection of the brain by measles virus (seen many years after the initial infection)
Destruction of grey and white matter
Progressive multifocal leukoencephalopathy
Associated with reactivation of the JC virus in white matter, usually due to immunosuppression
Progressive neurologic signs, leading to death
What are the causes of “locked in” syndrome?
Central pontine myelinosis
Basilar artery occlusion
Where are low sound frequencies heard best? High sound frequencies?
Low - apex of the cochlea (helicotrema)
High - base of the cochlea (near oval window)
Conductive hearing loss vs sensorineural hearing loss
Conductive
Rinne test is abnormal (bone>air)
Weber test localizes to the affected ear
Sensorineural
Rinne test is normal (air > bone)
Weber test localizes to the unaffected ear
Blink reflex
CN V1 in (unilateral)
CN VII out (bilateral)
Both eyes should blink
Pupillary reflex
CN II in (unilateral)
CN III out (bilateral)
Both pupils should constrict
Facial lesions (UMN vs LMN)
UMN: contralateral lower face paralysis with forehead sparing (because there is bilateral innervation to the upper face)
LMN: ipsilateral upper and lower facial paralysis
Horner Syndrome
Disruption of the sympathetic fibers of the face (any lesion above T1)
“PAM is horny”
Ptosis, anhydrosis, miosis”
What visual field defect does a pituitary adenoma cause?
Bitemporal hemianopia - due to compression of the optic chiasm, which affects the nasal fibers
Can also be caused by a craniopharyngioma in a child
Role of VEGF in eye pathology
Causes proliferation of new blood vessels that are thin and fragile (break easily)
Seen in proliferative diabetic retinopathy and in proliferative macular degeneration
Patient presents with painless progressive vision loss starting with night blindness
Retinitis pigmentosa (inherited retinal degeneration)
the rods are affected first, causing night blindness
Thalamus: VL
Input from basal ganglia and cerebellum
Output to motor cortex
Thalamus: VPL
Input from spinothalamic and medial lemniscus tracts (spinal component)
Output to somatosensory cortex (pain, temp, pressure, touch, vibration)
Thalamus: VPM
Input from spinothalamic and medial lemniscus tracts (tigeminal component)
Output to somatosensory cortex (face sensation, taste)
VPM* – Makeup goes on the face
Thalamus: MGN
Input from superior olive and inferior colliculus (auditory)
Output to auditory cortex (temporal lobe)
M = music = auditory
Thalamus: LGN
Input from optic tract (CN II)
Output to visual cortex (calcarine sulcus of the occipital lobe)
L = look = optic
Thalamus: AN
Input from Mammillothalamic Tract
Input to cingulate gyrus
Hypothalamus: supraoptic nucleus
Makes ADH
Hypothalamus: paraventricular nucleus
Makes oxytocin
*think gravida-para(ventricular) –> make breast milk when pregnant
Hypothalamus: lateral area
Drives hunger
Damage causes anorexia
Hypothalamus: Ventromedial area
Drives satiety
Damage causes obesity
Anterior hypothalamus
Cooling (A/C)
Parasympathetic
Posterior hypothalamus
Heating
Sympathetic
Hypothalamus: suprachiasmatic nucleus
Circadian rhythm
Release of melatonin from pineal gland
(you need sleep to be charismatic)
A tumor is found in the cerebellum of a 4 year old child
Medulloblastoma
Neuroectodermal tumor
Homer-wright rosettes on histology
Poor prognosis: spreads via CSF and can metastasize to the cauda equina “drop metastases”
M = metastases
A tumor is found in the 4th ventricle of a 5 year old child
Ependymoma
Arises from ependymal cells (lining of the ventricles)
Can block CSF and cause hydrocephalus
Perivascular rosettes on histology
Cyst with a mural nodule on a head CT of a child
Pilocytic astrocytoma
Arises from astrocytes (GFAP+)
Rosenthal fibers (hair-like corkscrew fibers)
Benign, good prognosis
What brain tumor has whorled cellular appearance and psammoma bodies?
Meningioma
psammoMa bodies
Patient presents with hearing loss and tinnitus in one ear and a mass is suspected. What is it and where is it likely located?
Schwannoma located at the cerebellopontine angle
Benign tumor of schwann cells that is commonly located on CN 8
S-100 positive (neural crest origin)
**Bilateral schwannomas are associated with NF-2
Bilateral CN 8 Schwannomas is seen in what pathology?
Neurofibromatosis type 2
Patient presents with seizures. CT reveals calcified tumor in the white matter of the frontal lobe
Oligodendroglioma
Round nuclei with clear cytoplasm - fried egg appearance
Where do metastatic brain tumors most commonly originate from?
Breast, lung, and kidney neoplasms
Brain tumor on CT crosses the corpus collusum, has necrotic areas surrounded by pseudopalisading cells
Glioblastoma multiforme
Astrocytic origin (GFAP +) 1 year median survival
What layers do you cross when performing an LP? Where do you perform an LP?
Skin, ligaments, epidural space, dura, and arachnoid → DO NOT cross the pia
Between L3 and L4 or L4 and L5, level of the iliac crest
“To keep the cord alive, keep the spinal needle between L3 and 5”
What areas in the brain are particularly susceptible to ischemia?
The hippocampus is the first area affected by ischemia!
Pyramidal neurons of the hippocampus (temporal lobe) that are important in long term memory
Purkinje layer of the cerebellum – integrates sensory perception with motor control
Pale infarct vs hemorrhagic infarct
Pale infarct = thrombotic stroke (no blood flow)
Hemorrhagic infarct = embolic stroke, usually from the left side of the hear (originally no blood flow but then blood flow resumes)
How do opioids work?
Prevent release of pain neurotransmitters (glutamate, substance P) by binding to opioid receptors (GPCRs)
Prevent influx of Ca2+ into the presynaptic terminal and open K+ channels for K+ efflux (leading to hyperpolarization)
Also act at the postsynaptic terminal by opening K+ channels for K+ efflux
Broca’s area
Inferior frontal gyrus of frontal lobe
Nonfluent aphasia with good comprehension, poor repetition
“Broken boca”
Wernicke’s area
Superior temporal gyrus of the temporal lobe
Fluent aphasia with impaired comprehension and repetition
“Wernicke is Wordy but makes no sense”
Conduction (aphasia)
Damage to arcuate fasciculus.
Poor repetition but fluent speech, intact comprehension.
Global aphasia
Nonfluent aphasia with impaired comprehension (Broca’s, Wernicke’s and arcuate fasciculus all affected)
CN X lesion
Uvula deviates AWAY from the side of the lesion
Weak side collapses and the uvula points away
CN V motor lesion
Jaw deviates toward the side of the lesion due to unopposed force from the opposite pterygoid muscle
CN XI lesion
Weakness turning head to side away from lesion (Left sternocleidomastoid is responsible for turning head to the right)
Shoulder droop on affected side (trapezius)
CN XII lesion
Tongue deviates TOWARD the lesion due to weakened muscles on the affected side
(“lick your wounds”)
Kluver-Bucy syndrome
Lesion to the bilateral amygdala (within the temporal lobe) that causes disinhibited behavior (hyperphagia, hypersexuality, hyperorality)
Associated with HSV-1
Wernicke Korsakoff Syndrome
Lesion to the bilateral mammillary bodies, associated with thiamine B1 deficiency and excessive EtOH use
Wernicke problems come in a CAN of beer: Confusion, Ataxia/Amnesia, Nystagmus
Treacher-Collins Syndrome
Abnormal development of the 1st and 2nd branchial arches – mandibular hypoplasia, small ears, abnormal styloid process, problem with stapes
Tetanus toxin
Botulism toxin
Tetanus: Tetanospasmin blocks the release of inhibitory neurotransmitters, GABA and glycine, from Renshaw cells in the spinal cord
Botulism: Prevents the release of Ach from the neuromuscular junction
5 year old presents with repeated sinopulmonary infections, sensitivity to light, and difficulty walking… what do you suspect?
Ataxia-telangectasia
A genetic defect in DNA double stranded break repair that causes cerebellar atrophy and immunodeficiency (due to IgA deficiency)
Patient presents with intellectual disability, large ears, prominent jaw, large testes
Fragile X syndrome
An X linked defect causing hypermethylation and inactivation of the FMR1 gene – trinucleotide repeat (CGG)
“Xtra large ears, testes, and jaw, X linked”
Newborn presents with enlarging head circumference
Due to hydrocephalus- head enlarges since the sutures aren’t fused yet
Suspect cerebral aqueduct stenosis- CSF is unable to flow from the third ventricle to the 4th ventricle
Dandy-Walker Malformation
Congenital failure of the cerebellar vermis to develop. Present with massively dilated 4th ventricle and absent cerebellum
CT of an infant shows displacement of the brainstem through the foramen ovale
Arnold-Chiari malformation (Chari type II)
Almost always associated with meningomyelocele
What does increased acetylcholinesterase in the amniotic fluid suggest?
Neural tube defect
Also see increased alpha fetoprotein in amniotic fluid and in maternal serum
**Dec AFP = down syndrome
Where is the spinal lesion? Patient has a loss of pain and temperature sensation of the upper extremities but touch is intact
Syringomyelia: lesion to the anterior white commissure of the spinothalamic tract within C8-T1
Where does poliomyelitis injure the nervous system?
In the anterior motor horn of the spinal cord.
Causes lower motor neuron symptoms: weakness, dec DTRs, atrophy)
Werdnig-Hoffman disease
Inherited degradation of the anterior motor horn – presents as a floppy baby who dies within a few years
Similar to polio
If a patient presents with symptoms of UMN and LMN problems, what should you suspect?
Amyotrophic Lateral Sclerosis (ALS)
Aka Lou Gherig’s disease
Degenerative disorder of the UMN and LMN of the corticospinal tract
What causes ALS?
Typically sporadic
In familial cases it is due to a mutation in superoxide dismutase, leading to free radical damage
Friedrich Ataxia: what causes the damage? What are symptoms?
Trinucleotide repeat disorder (GAA) in the frataxin gene that leads to impaired mitochondrial function and free radical damage, leading to degeneration of the cerebellum and spinal tracts
Ataxia, loss of DTRs, frequent falling, diabetes mellitus, pes cavus, and hypertrophic cardiomyopathy
Presents in childhood with kyphoscoliosis
“Friedrich is your Frat(axin) brother: he’s always staggering and falling but has a sweet, big heart”
Appears similar to vitamin E deficiency
Damage to what nerve causes vertical diplopia?
CN IV
Will have trouble looking down - walking down stairs or reading a book
Damage to what nerve causes ptosis? What else will you see?
CN III
Will cause a “down and out” eye
Damage to what nerve causes horizontal dipolopia?
CN VI
Basal Ganglia: Indirect pathway
NO GO pathway: inhibits movement
Dopamine inhibits this pathway (via D2 receptors) to facilitate movement
Basal Ganglia: Direct pathway
GO pathway: facilitates movement
Dopamine activates this pathway (via D1 receptors) to facilitate movement
Direct and indirect pathways in Parkinson’s
Hypokinetic disorder
Inc indirect pathway, dec. direct pathway
Due to loss of dopamine from the substantia nigra
S/S: resting tremor that improves with movement, rigidity, akinesia (difficulty initiating movement), shuffling gait
Direct and indirect pathways in Huntington’s
Hyperkinetic disorder
Inc direct pathway, dec indirect pathway
Due to loss of GABA and Ach. Increased dopamine.
Trinucleotide repeats (CAG)
What causes Huntingtons
Autosomal dominant mutation on chromosome 4 that consists of CAG trinucleotide repeats
What prenatal lab result suggest Down Syndrome or other chromosomal abnormality?
Decreased AFP
Pick’s disease histo
Atrophy of the frontal lobe causing personality changes
Tau protein inclusions
Most common cause of recurrent spontaneous lobar hemorrhage in older?
Cerebral amyloid angiopathy
seen in elderly patients with recurrent lobar hemorrhage – due to B amyloid deposition in the walls of cerebral arteries → causing rupture
Damage to subthalamic nucleus causes what clinical picture?
What usually causes this?
Contralateral hemiballismus
Usually due to a lacunar infarct
Therapeutic hyperventilation
(used to treat acute cerebral edema) – hyperventilation blows off CO2 which causes constriction of the vessels and dec blood flow → dec in intracranial pressure
Berry aneurysm where will lead to CN 3 damage?
To the posterior cerebral artery or the superior cerebellar artery
Compress CN 3 and cause damage!
What type of necrosis does the brain undergo?
Liquefactive necrosis
What meds can you give to decrease aqueous humor production?
B blockers (Timolol) a agonists (Brimonidine) carbonic anhydrase inhibitors (Acetazolamide)
What drugs can you give to increase outflow of aqueous humor in glaucoma?
M3 muscarinics (Pilocarpine) Prostaglandin agonists (Latanoprost)
Patient presents with a red and painful eye that developed suddenly. He also has a frontal headache. What do you suspect?
Closed angle glaucoma- When the peripheral iris pushes up against the trabecular network and prevents aqueous humor from draining
OPHTHALMIC EMERGENCY!
Mitochondrial Myopathies
Can only be passed on by mom:
Myoclonic epilepsy with ragged red fibers (MERRF) – myoclonic seizures and myopathy associated with exercise. Blotchy red muscle fibers on Gomori trichrome stain
Leber optic neuropathy (bilateral vision loss)
Mitochondrial encephalopathy with stroke like episodes and lactic acidosis (MELAS)
Kinesin vs Dynein
Kinesin: carries proteins along microtubules in an anterograde fashion (from cell body to axon terminal)
Dynein: carries proteins along microtubules in a retrograde fashion (from axon terminal to cell body)
What drug is used in the treatment of status epilepticus? What else can it be used for?
Benzodiazepines (inc GABA action via enhanced postsynaptic Cl- influx)
Safe to use in pregnancy
Used for delirium tremens, night terrors, sleepwalking, general anesthetic, insomnia
What drug is used for the treatment of absence seizures?
Ethosuximide (blocks thalamic T type Calcium channels)
It SUX to have absence seizures
What anti-epileptic drug is first line in neonates?
Phenobarbital (Inc GABA action by increasing duration of Cl channel opining)
Pheno-dura-tal = duration of channel opening
Pheno-baby- tal
First line tx for acute tonic clonic seizure?
Valproic Acid (Inc Na channel inactivation, inc GABA concentration by inhibiting GABA transaminase)
What drug is used for simple or complex partial seizures?
Carbamazepine (blocks Na channels)
Bring carbs to a party!
Severe hypotension (ie cardiogenic shock) can lead to what type of brain pathology?
Wastershed zone damage (between MCA-ACA and MCA-PCA)
Brain biopsy of HIV dementia – what cells are infected?
Gross atrophy
Microglial nodules
Damage due to cytokine release
Microglia are infected
Calcified intracranial mass in a child that causes visual disturbances and is full of brown-yellow fluid with cholesterol crystals?
Craniopharyngioma
What brain tumor can produce EPO and cause polycythemia?
Hemangioblastoma
What drug can precipitate opioid withdrawal symptoms?
Buprenorphine (Pre-tends to be like m-orphine)
It is a partial opioid agonist that can act like an antagonist in the presence of full opioid agonists – can precipitate withdrawal
What nerve is targeted in Bell’s palsy?
The facial nerve (CN 7)
What drug is first line for trigeminal neuralgia?
Carbamazepine
What drug is used for treatment of myoclonic seizures?
Valproic acid
Patient presents with tremors and difficulty walking, as well as personality changes. He has had some vision problems. Patient has elevated serum transaminases. What is the disease and how should it be treated?
What is the inheritance pattern?
Wilson disease – deposition of copper in the liver, eye, and brain (the putamen and globus pallidus)
Treat with D-penicillamine
Autosomal recessive
Trinucleotide repeat disorders
o Fragile X Syndrome: CGG
o Friedrich ataxia: GAA
o Huntingtons: CAG
o Myotonic dystrophy: CTG
“eX Girlfriend’s First Aid Helped Ace My Test”
Depolarizing neuromuscular agent(s)
Succinylcholine: strong ACh receptor agonist – produces sustained depolarization and prevents muscle contraction
Reverse with Dantrolene
Nondepolarizing neuromuscular agents
Tucocurarine, pancuronium, rocuronium
Competitive ACh antagonists that cause paralysis
Reverse with neostigmine
Reflexes
Biceps
Triceps
Patella
Achilles
o Biceps = C5
o Triceps = C7
o Patella = L4
o Achilles = S1
What vitamin deficiency does Friedrich Ataxia resemble?
Vitamin E deficiency
neurologic problems due to demyelination (ataxia, dysathria, lower limb arreflexia, peripheral neuropathy)
Noise induced hearing loss results in what damage?
trauma to the stereociliated hair cells of the organ of Corti
Excess of what vitamin is associated with pseudotumor cerebri? (Idiopathic intracranial HTN)
Vitamin A
Communicating vs noncommunicating hydrocephalus
o Communicating: dec CSF absorption by arachnoid granulations (eg scarring post meningitis) leading to inc intracranial pressure
o Noncommunicating: structural blockage of CSF circulation (eg tumors, aqueductal stenosis) leading to inc ICP
Causes of vertigo
- Meniere disease: increased pressure and volume of endolymph in the inner ear leading to recurrent episodic vertigo, sensation of ear fullness or pain, and unilateral hearing loss/tinnitus
- Benign paroxysmal positional vertigo: otoliths in the semicircular canal lead to brief episodes brought on by head movement, no auditory symptoms
- Vestibular neuritis: inflammation of the vestibular nerve, single episode that can last days, severe vertigo but no hearing loss
Patient presents with papilledema, headache, and vomiting. On exam you notice paralysis of upward gaze, ptosis, and pupillary abnormalities. Head CT shows an intracranial tumor. What do you suspecT?
Pineal gland mass:
causes obstructive noncommunicating hydrocephalus from aqueductal stenosis (papilledema, headache, and vomiting) and dorsal midbrain aka Parinaud syndrome (paralysis of upward gaze, ptosis, and pupillary abnormalities) due to direct compression of the pretectal region of the midbrain.
Patient presents with a pure motor or pure sensory UMN defect. What should you suspect?
Lacunar infarct: due to HTN, involve the small penetrating vessels that supply the deep brain structures and subcortical white matter
Vessels develop arteriolar sclerosis and may become occluded → development of small cavitary lesions due to liquefaction (tissue loss surrounded by gliosis)
Vitamin B12 deficiency has what effect on the spinal cord?
Loss of the dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts "SCD" Spinocerebellar Corticospinal Dorsal columns
Histology of Alzheimer’s? What neurotransmitter is deficient and why?
neurofibrillary tangles (tau) and senile plaques (B-amyloid)
ACh is deficient due to a deficiency of choline acetyltransferase
Histology of Parkinsons
Lewy bodies: composed of a-synuclein (intracellular eosinophilic inclusions)
Brain biopsy shows intracytoplasmic vacuolizations of neurons in gray matter (spongioform transformation). What does this patient have and what is a common clinical presentation?
Creutzfeldt Jakob disease- Prion disease. Rapidly progressive dementia with myoclonus
Prions = beta pleated sheet that are resistant to proteases and accumulate in the brain
What does a step-wise decline in cognition suggest? What about a gradual decline?
Step-wise = vascular dementia (second most common cause of dementia)
Gradual = Alzheimers (most common cause of dementia)
What part of the brain does wilson disease affect?
The putamen and globus pallidus– causes hyperkinetic movements
What part of the brain does huntington’s affect?
The caudate nucleus
Where does intraventricular hemorrhage occur in neonates? What can be done to help prevent this?
Bleeding most often originates from the germinal matrix, which is a region adjacent to the lateral ventricle and it contains proliferating cells (neurons and glial cells migrate out during brain development)
Important to give neonates a shot of Vitamin K (since they are deficient and this will help with coagulation)
Which inhaled anesthetics have a faster onset of action?
Those with low blood solubility (low partition coefficient)
Charcot Bouchard aneurysm rupture
in the lenticulostriate arteries, due to chronic HTN, hemorrhage involves the deep brain structures (basal ganglia, cerebellar nuclei, thalamus, pons)
Why are people with Down Syndrome more at risk of developing Alzheimers?
APP (amyloid precursor protein) is located on the long arm of chromosome 21 and a mutation in this gene can lead to Alzheimer’s
People with Down Syndrome have three copies of chromosome 21 and therefore produce higher levels of APP
Posturing in head injury patients
o Decorticate (flexor): damage to upper midbrain o Decerebrate (extensor): damage to upper pons
Damage to nondominant parietal cortex?
Damage to dominant parietal cortex?
Nondominant: hemispatial neglect syndrome
Dominant: agraphia, acalculia, finger agnosia, left-right disorientation
Damage to cerebellar hemisphere
Intention tremor, limb ataxia, loss of balance
Damage causes ipsilateral deficits!
Damage to cerebellar vermis
Truncal ataxia, dysarthria
Cavernous sinus syndrome:
due to infection of the sinuses (ethmoid or sphenoid) or teeth that spreads to the cavernous sinus
o Patients present with headache, fver, proptosis, and ipsilateral defects in CN 3, 4, 6, and V1/2
