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244 Cards in this Set

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Where do each of the cranial nerves III-XII emerge from?
III (oculomotor)- recess between pons and midbrain

IV (trochlear)- emerges from dorsal surface of brain stem

V (trigeminal)- pons

VI, VII, VIII- junction of pons and medulla

IX, X, XII- medulla

XI- ventral roots of spinal cord
The brain is made of the forebrain, the midbrain and the hindbrain. What makes up these areas?

What makes up the brainstem?
Forebrain:
1. telencephalon- neocortex, hippocampus, internal capsule
2. diencephalon- thalamus, hypothalamus

Midbrain:
1. superior colliculus
2. inferior colliculus

Hindbrain:
1. cerebellum
2. pons
3. medulla

Brainstem: midbrain, pons, medulla
What does the longitudinal fissure divide?
Splits the brain into right and left halves
What is the central sulcus? What functions do the pre and post central gyrus have?
The central sulcus seperates the fronal lobe from the parietal lobe

The precentral gyrus is found in the frontal lobe and is responsible for motor function

The postcentral gyrus is found in the parietal lobe and is responsible for somatosensory function
Where is Wernicke's Area? What is it associated with?
Wernicke's area is in the superior temporal gyrus.

Damage to this area leads to fluent aphasia with impaired comprenension
Where is Broca's Area? What is it associated with?
Broca's area is in the inferior frontal gyrus.

Damage to this area leads to nonfluent aphasia with intact comprehension.
The brain comes from what embryologic epithelium (ectoderm, endoderm or mesoderm)?

Please give the 3 vesicle stage --> the 5 vesicle stage --> adult derivatives
Initial 3 Vesicle Stage: prosencephalon, mesencephalon, rhombencephalon

5 Vesicle Stage:
Telencephalon
Diencephalon
Mesencephalon
Metencephalon
Myelencephalon

Adult Derivatives:
Telencephalon --> cerebral hemispheres
Diencephalon --> thalamus/hypothalamus
Mesencephalon --> midbrain, superior colliculus, inferior colliculus
Metencephalon --> pons, cerebellum
Myelencephalon --> medulla
How are cell bodies in the ventral horn arranged?

(sp. flexors, extensors, proximal, distal)
Cell bodies in the ventral horn are loosely arranged so that neurons innervating flexors are more lateral in teh gray matter while neurosn innervating extensors are more medial.

Neurons innervating more distal muscles are more ventral than are neurons innervating more proximal muscles.
What changes occur at the levels of T6 and T7 in the spinal cord?
The posterior funiculus on each side is divided by the posterior intermediate septum above T7 into two seperate fasiculi:

1. fasciculus gracilis (medial)- present at all spinal levels, contains long ascending branches from fibers from sacral, lumbar and lower 6 thoracic dosal roots
2. fasciculus cuneatus (lateral)- first appears around T7, contains long ascending brances of fibers from upper 6 thoracic and all cervical dorsal roots

As fibers from higher levels of the cord enter the posterior funiculus, they assume a more lateral position --> this provides an organization to the posterior funiculus such that sacral fibers are most medial, cervical fibers are most lateral and lumbar/thoracic fibers occupy intermediate positions
What is the dorsal column/medial lemniscus pathway? What are the sensory receptors involved?
Carries information concerned wtih fine touch, proprioception and vibration

Pacinian corpuscles, joint receptors, Meissner's corpuscles, GTO, muscle spindles
A Pacinian corpuscle is activated. Where would the fibers go if the corpuscle was in the right leg? The right arm?
DORSAL COLUMN MEDIAL LEMNISCUS PATHWAY

The lower extremities use the fasiculus gracilis

The upper extremities use the fasiculus cuneatus

First order neurons carry information from periphery up the fasciculus gracilus/cuneatus and synapse in the nucleus gracilus/cuneatus on the ipsilateral side

Second order neurons decussate in the medulla, ascend contralaterally in the medial lemniscus and synapse on in the VPL (ventral posterior lateral nucleus- body sensation)

Third order neurons travel up the posterior limb of the internal capsule and synapse on the somatosensory cortex
If your right finger was burned, what path would the fibers travel to get to your brain?
ANTERIOR LATERAL SYSTEM (aka spinothalamic tract)

First order neurons carry information into the spinal cord from peripheral temperature (A delta and C fibers) receptors via the dorsolateral tract (remember these neurons split and travel 1-3 segments up and down the cord to amplify the signal) and synapse on second order neurons on the ipsilateral side

Second order neurons immediately cross the cord in the ventral white commissure and travel up in the lateral spinothalamic tract to synapse in the VPL of the thalamus (ventral posterior lateral nucleus- body sensation)

Third order neurons then travel the posterior limb of the internal capsule and synapse on the somatosensory cortex
What tract is responsible for vibration, fine touch, proprioception and pressure of the body?
Dorsal Column Medial Lemniscus Pathway
What tract is responsible for pain and temperature of the body?
Anterior Lateral Spinothalamic Tract
Please describe the pathway responsible for orofacial fine touch and vibration?
First order neurons carrying information come in via the trigeminal verve and synapse in the cheif sensory nucleus

Second order neurons send out two projections (one ipsilateral and one contralateral) up the brainstem to synapse in the VPM (ventral posterior medial nucleus- facial sensation) in both halves of the thalamus

Third order neurons move up on each side and synapse on the somatosensory cortex
Please describe the pathway responsible for orofacial pain and temperature?
First order neurons carry pain and temperature information (A delta and C) through the trigeminal nerve and synapse in the spinal trigeminal nucleus in multiple places (to amplify the signal)

Multiple second order neurons leave the spinal trigeminal nucleus, cross to the ipsilateral side in the medulla and travel up to synapse in the VPM of the ipsilateral thalamus

Third order neurons travel up the posterior limb of the internal capsule to synapse on the somatosensory cortex
What type of visual information does the right optic tract carry?

What if you severed this tract??
Right optic tract carries visual information from the left visual field.

If you severed the right optic tract, homonymous hemianopia (loss of half of each of the R and L visual fields)
An 8 year old boy riding his bike without his helmet on, falls backward and hits his posterior occiput on the pavement. What deficit in vision would you expect?
Central Scotomas (dark spots on fovea)
80% of the optic tract neurons (second order neurons) synapse on the lateral geniculate body and then send their third order neurons on towards the calcarine fissure.

What is the calcarine fissure and what is its organization?
The calcarine fissure horizontally divides the occipital lobe. The cortical area withing and directly around the calcarine fissure is the primary visual cortex.

The upper bank of the calcarine fissure gets contralateral lower visual quadrant information.
The lower bank of the calcarine fissure gets contralateral upper visual quandrant information.
Briefly explain the basics of the corticobulbospinal tract.

What are the anterior and lateral corticospinal tracts?

What is the corticobulbar tract (ie where does it synapse)?
Cell bodies in the cerebral cortex (pre central gyrus) descend through the CNS and make synapses in the brainstem (corticobulbar) and in the ventral spinal cord (corticospinal)

The anterior corticospinal tract is responsible for movement of the axial muscles.

The lateral corticospinal tract is responsible for movement of the extremities.

The corticobulbar tract synapses on the red nucleus, CN III, IV, V, VI, VII, IX, X, XI and XII
Most neuronal activity of the basal ganglia occurs before a particular movement begins. What makes up the basal ganglia?
The basal ganglia consists of the neostriatum (caudate nucleus and putamen) and the paleiostriatum (globus pallidus)
What is the excitatory/direct pathway of the basal ganglia?
The net result of activation of the direct pathway is increase output from the thalamus with a resultant increase in activation of the motor nurons of the cerebral cortex

Basically, the thalamus is always telling the motor to GO! Globus Pallidus medius is normally inhibits the thalamus, but the neostriatum (aka caudate and putamen) inhibit the inhibitor, allowing the thalamus to stimulate the corticobulbar spinal tract and stimulate movement
What is the inhibitory/indirect pathway of the basal ganglia?
When th eindirect basal ganglia pathway is activated, the result is decreased activity of the thalamus and therefore decreased activity of the motor regions of the cerebral cortex. STOP A MOVEMENT.
How does Parkinson's affect the Direct/Excitatory and Indirect/Inhibitory basal ganglia pathways?
Direct: Substantia nigra normally releases dopamine that binds to D1 (excitatory) receptors, stimulating the pathway (increasing motion).

Inhibitory: Substantia nigra usually releases D2 (inhibitory), inhibiting the inhibitory pathway (increasing motion)

In Parkinson's, there is a loss of dopamine (motion is decreased)
How is visual acuity recorded? What cranial nerve are we testing?
CN II- Optic nerve

20 feet away for a wall chart
14 inches away for a hand held chart

The acuity is the last line correctly read.

Test one eye at a time
The left optic tract contains visual information from where?

If the left optic tract were cut, what would the visual deficit be?
Information from the right visual field.

Homonymous hemianopia of the right side.
How are the pupils constricted?
PARASYMPATHETIC INNERVATION

Light hits the first order bipolar neuron --> travels back and synapses on the pretectal nucleus --> bilaterally projects to both the ipsilateral and contralateral edinger westphal nucleus --> synapses in the ciliary ganglion --> constrict the pupillary radial muscle

both pupils should contract bilaterally (consentual reflex)
How are the pupils dilated?

How is this pathway affected in Horners Syndrome?
SYMPATHETIC INNERVATION

First order neuron comes from ipsilateral hypothalamus and travels down the spinal cord --> synapses in the IML of the ventral horn at T1 and travels up the sympathetic chain --> synapses on the superior cervical gangion --> third order neuron travels out V1 to the pupil to dilate it

Because when the first order neuron travels down the spinal cord and synapses near T1 and then has to travel back up the to the superior cervical ganglion, it has to travel through the apex of the lung (presumably where the tumor is), thus cutting off sympathetic activity to that side --> pupil will not be able to dilate on the side with the pancoast lesion
Which cranial nerves control the extraocular muscles? What is the action of each extraocular muscle?
LR6 SO4, all others CN III

Medial rectus- adduction
Lateral rectus- abduction
Superior rectus- elevation and in
Inferior rectus- depression and out
Superior Oblique- depression and intorsion
Inferior Oblique- elevation and extorsion

*CN III also controls the levator palpebrae
What is the facial nerve (VII) responsible for?

How can we differentiate between an UMN lesion and a LMN lesion of the facial motor system? Is Bells Palsy an UMN or LMN lesion?
Facial nerve is responsible for all facial motor and taste to the anterior 2/3 of the tongue

Lesion of an UMN (ie first order before it reaches the facial nucleus) causes contralateral lower quadrant facial paralysis.

Lesion of a LMN (ie the facial nerve itself) results in ipsilateral facial paralysis.

The best way to distinguish this is to look for forehead wrinkling... if it is present on only one side --> lower motor neuron lesion; if it is present on both sides --> upper motor neuron lesion

Bells Palsy is a lesion of the LMN.
How is muscular strength graded?
Muscle strength is graded on the MRC Scale

5- normal power
4- able to contract the muscle against gravity and resistance
3- able to contract against gravity, but not resistance
2- able to contract only with gravity eliminated
1- a flicker
0- no contraction
What information does Rapid Alternating Movements provide?
Decreased amplitude and speed on side affected by pyramidal tract or extrapyramidal disease

Irregularity of amplitude, rhythm and placement in cerebellar disease
What is a positive Babinski Sign? What is this indicative of? When is a positive Babinski Sign normal?
Noxious scrape of lateral aspect of foot --> if big toe dorsiflexes, Babinski Sign is present --> indicative of UMN lesion

Normal in children up to 12-24 months
Pull out your visual lesion chart...
and pimp your partner :)
What is the basic pathway of an UMN and LMN circuit? How can you differentiate between an UMN and LMN lesion?
UMN leaves motor cortex and travels down pyramidal tract --> once it gets to the bottom of the brain stem/top of spinal cord it deccusates to the contralateral side --> travels down the spinal cord --> synapses at the correct levels --> LMN (alpha motor neuron) goes out to muscle

Characteristics of UMN weakness: clumsiness in greater proportion than loss of power, Babinski sign present (immediate), spasticity (delayed), increased tendon reflexes (delayed), little atrophy

Characteristics of LMN weakness: loss of power in greater proportion than clumsiness, hypotonia (flaccid limbs), muscle atrophy, muscle fasciculations
What are the three types of increased muscular tone?

Please describe them.
Muscle tone (UMN) in general is when the examiner moves the body in a specific way to see if there is any resistance.

Spasticity- UNIDIRECTIONAL increase in muscle tone (ie. as you stretch out bicep flexors you may have resistance, but as you stretch out tricep extensors, you have no resistance); involves anti gravity muscles; in upper extremities resistance in biceps, but not triceps; in lower extremities resistance in quadriceps but not hamstrings

Rigidity- BIDIRECTIONAL increase in tone to passive range of motion (can flex or extend), often seen in Parkinson's disease and other extrapyramidal disorders; resistance to passive ROM is independent of degree of force or rate of speed

Paratonia- BIDIRECTIONAL resistance to passive rage of motion that increases with force and rate of movement (as if they are preventing the movement on purpose, the harder you push, the more they push back); commonly seen in dementia
Myopathies can be either genetic or acquired. Please list them (don't explain yet)
Duchenne's Muscular Dystrophy- short arm of X chromosome

Facioscapulohumeral Muscular Dystrophy- long arm of chromosome 4

Limb Girdle Muscular Dystrophy- defects in multiple genes

Myotonic Dystrophy- centromere of chromosome 19

Polymyositis, dermatomyositis, viral, corticosteroid administration- acquired myopathies
What is the genetic defect in Duchenne's Muscular Dystrophy? Who is your typical patient? How does it present?
Duchenne's is a defect in the gene that codes for dystrophin on the short arm of the X chromosome --> leads to accelerated muscle breakdown; sex linked recessive

Typically presents in childhood in males

Initially, starts in the pelvic girdle and RAPIDLY progresses superiorly. Pseudohypertrophy of calf muscles d/t fibrofatty replacement of muscle, increased lordosis --> muscles are weak and can't hold spine erect, use of Gower's maneuver to stand up
What is the genetic defect in Facioscapulohumeral Muscular Dystrophy? Who is your typical patient? How does it present?
Key defect is on the long arm of chromosome 4 (AD)

Typically presents in adolescence in either males or females

Initially presents in the shoulder girlde and SLOWLY progresses to other areas. Ask the patient to push off from a wall --> will see atrophy and weakness of shoulder muscles, especially serratus anterior, resulting in winged scapula
What genetic defect is found in Limb Girdle Muscular Dystrophy? Who is your typical patient? How does it present?
Defects are found in multiple genes

Can present in any age or sex group

Can start in either the pelvis or the shoulder (so can still see bilateral wing of the scapula)
In a patient with an UMN lesion, what immediate signs would you look for? Delayed signs?
Babinski sign (immediate)
Spasticity (delayed)
Increased reflexes (delayed)
On a recent neuro exam, your 43 year old patient was unable to pick up a pencil. You do not see muscle atrophy as the cause. Is his lesion in the UMN or LMN?
UMN
What is the defect in Myotonic Dystrophy? What physical characteristics would you expect a patient with Myotonic Dystrophy to have?
A gene near the centromere of chromosome 19 codes for myotonic dystrophy protein kinase --> disease is d/t hundreds of CTG repeats in the gene

Patient would have frontal alopecia, myopathic (triangular) facies and wasting of the SCM, percussion myotonia of thenar eminence, when you go to shake their hand, they can't stop the grip

**he showed like 3 pictures of this**
Which muscular dystrophies are due to sex linked and autosomal mutations?
Sex linked: Duchennes

Autosomal: Facioscapulohumeral (AD), Motonic Dystrophy

Either: Limb- Girdle
Acquired myopathies include polymyositis and dermatomyositis. Please describe these, specifically what antibodies you would test for (from FA).
Polymyositis- progressive symmetric proximal muscle caused by CD8 T cell induced injury to myofibers; patient will usually come in because of shoulder weakness of because of upper leg muscle fatigue when walking (remember the picture of the little boy trying to lift his arms in the air)

Dermatomyositis- similar to polymyositis, but also involves a maylar rash, a heliotrope rash and grottons papules (pink patches on knuckles)

Both can be tested for in the lab --> positive ANA and anti Jo 1
What is the basic difference between genetic and acquired myopathies as far as which muscles are affected?
Genetic affects more proximal muscles

Acquired affects more distal muscles

THIS IS GENERAL
What happens in Myasthenia Gravis? How would you confirm this diagnosis? As soon as you make the diagnosis, what is your next step?
Autoantibodies to postsynaptic AChR causing ptosis, diplopia and general weakness (proximal > distal). Symptoms worsen with continued muscle use (fatiguing weakness). Deep tendon reflexes remain intact.

Edrophonium temporarily relieves muscle weakness by inhibiting AChE so more ACh is available to stimulate the receptors.

As soon as you make the diagnosis, all MG patients get a chest XR or CT to rule out THYMOMA or THYROID DISEASE
What is the difference between polyneuropathy and multiple mononeuropathies?
Polyneuropathy is bilaterally symmetric (commonly stocking and glove). Areas of sensory loss do not match up with known territories of individual nerve bundles.

Multiple mononeuropathies are when there are multiple impairments that can all be traced back to a single identifiable nerve bundle.
Patient comes in with numbness and weakness in their hands and feet. What is going on? What could have caused this?
Polyneuropathy

Distal > proximal weakness and numbness

Common causes of Polyneuropathy are: DM, EtOH, genetic, lead poisoning (purely motor, remember wrist drop), arsenic poisoning (purely sensory), Guillain Barre, cisplatin, vincristine, isoniazid
Which motorneuron disease is characterized by maximum stress in the brainstem?
Progressive Bulbar Palsy
This motorneuron disease mostly affects babies. Where is the maximum stress?
Spinal Muscular Atrophy --> sp. Werdnig Hoffman; LMN stress

Baby will present with 'frog legs', no reflexes, head lag, respiratory atrophy,
What is the difference between primary and secondary headaches? Please provide examples of each?
Primary headache is when the headache IS the disease. Includes, tension type, migraine, cluster

Secondary headache is when the headache is a symptom of the disease. Includes HA d/t vascular complications, trauma, neoplasm, infection, inflammation and toxins.
What factors would tip off a physician that a patient was suffering from migraine headaches? What qualifications do migraines have to meet for diagnosis?
Recurrent headaches(5) lasting 4-72 hours with at least two of the following characteristics:

unilateral location, pulsating quality, inhibits/prohibits daily activity, aggravated by a routine physical activity (walking upstairs), nausea, vomiting, photophobia, phonophobia

May include symptoms of aura (lasting between 4-60 minutes)

**the three highly predictive screens for migraine are nausea, disability and photophobia**
What factors would tip off a physician that a patient was suffering from tension type headaches?
At least 10 HA episodes lasting 30 minutes to 7 days with a pressing/tightening quality (nonpressing), bilateral, NO aggravation by physical activity, NO nausea/vomiting, NO photophobia/ phonophobia
What factors would tip off a physician that a patient was suffering from cluster headaches?
'Cluster' means clustering in time, not in location

Attacks are brief, but intense

The pain always stays on the same side of the head, always near an orbit

*one of the few headache disorders that affects M>F*
What factors would tip off a physician that a patient was suffering from medication over use headaches? What medications could cause this?
Pain is usually worse on wakening, and goes away as soon as they take their medicine

The HA occurs EVERYDAY

The example he gave was tryptan --> if you take them for a prolonged period of time, you can get analgesic rebound headaches
What factors would tip off a physician that a patient was suffering from giant cell arteritis headaches? What is necessary to diagnose this?
Normally, the temporal arteries will be swollen, indurated and tender. We will take a biopsy from these (because apparently they are not important) and will see a GIANT CELL surrounded by inflammation
What factors would tip off a physician that a patient was suffering from brain tumor headaches?
The pain does not come and go, nor does it get better over the course of up to a year
In the US population, what is the most common chronic disorder?
MIGRAINES :( :( :(
What are the clinical signs of an aneurysm rupture in the brain?
Sudden onset of severe headache

Stretch signs of irritation (blood on CSF)
What is 'aura'? How would migraines with and without aura differ?
Visual aura- scotomas (blindpots), photopsia (flashes), fortification spectra (zig zag lines)

Somatosensory aura- unilateral paresthesias

Motor aura- hemiparesis

Language aura- aphasia

In a patient with a migraine aura, the auras will start before the pain
How will the pain complaints differ between a migraine, tension HA, cluster HA, and brain tumor?
Migraines present sporadically and resolve sporadically (may once/month)

Tension headaches present with a chronic intensity that doesn't change or resolve over time

Cluster headaches present with multiple intense attackes over a month or two but then resolve for a few months

Brain tumor has progressively worsening pain over the course of many months (up to a year)
The anterior cerebral artery supplies...

The middle cerebral artery supplies...

The posterior cerebral artery supplies...
ACA supplies anteromedial surface

MCA supplies lateral surface

PCA supplies posterior and inferior surfaces


Off of these large arteries are the penetrating arteries into the tissue itself

see FA p 400 and review circle of Willis
How does blood get from your heart to your brain???

Don't get cranky...
Brain has four main arteries of supply:

Two internal carotids --> give off anterior cerebral artery, middle cerebral artery, anterior chorioidal artery, posterior communicating artery

Two vertebral arteries arise from the two subclavian arteries and ascend the neck within the upper six cervical vertebra, enters the skull and gives rise to the posterior inferior cerebellar artery and then combine into the basilar artery --> the basilar artery gives off the pontine arteries, anterior inferior cerebellar arteries, superior cerebellar arteries and posterior cerebral artery
What is a subarachnoid hemorrhage? How would this appear on a CT scan?
Subarachnoid hemorrhages typically result from a ruptured aneurysm (usually a Berry aneurysm).

Patient will say that this is 'the worst headache of my life' (FA)

Bloody or yellow spinal tap.

If you catch this early (which you will d/t severe pain), the fresh blood will absorb x rays d/t the high concentration of Hb and appear WHITE on a CT
What are small vessel aneurysms called?
Charcot Bouchard microaneurysms in the penetrating arteries
What is an intraparenchymal hemmorage? Where does it typically occur? What is it normally due to? How will this appear on a CT?
Normally, intraparenchymal hemorrhages are HTN or arteriovenous malformation associated.

Typically occur in basal ganglia, internal capsule or lobar white matter.

Occurs with rapid accelerations and decelerations

On a CT, the fresh blood will show up as bright white.
What artery supplies the pre and post central gyri? What are these gyri responsible for again?
Precentral gyri- motor cortex

Postcentral gyri- sensory cortex

Middle cerebral artery supplies these
Which artery supplies Wernicke's area? Broca's area? What may happen if there is an embolis and blood supply is cut off to these areas?
Wernicke's is supplied by the middle cerebral artery- fluent aphasia with no comprehension

Broca's area is supplied by the middle cerebral artery- nonfluent aphasia with comprehension
What vein is most likely to thrombose?
superior saggital sinus
What are the differences between thrombotic and embolic infarctions in the brain?

How long can the brain tissue go without fresh blood?
Thrombosis refers to the occlusion of a vessel lumen by static means (ie a plaque).

Embolism is occlusion of a vessel d/t a mobile plaque thrown off of a thrombus that gets caught in a lumen. Most embolisms come from atrial fibrillation.

There will be a clot that will give off a wedge shaped area of infarct.

Irreversible damage after 5 minutes.
Irreversible neuronal damage after 12-48 hours.
Necrosis after 12-72 hours.
What are lacunar infarctions?
Lacunar infarctions are caused by occlusion of smaller, penetrating arteries.
What are the risk factors for atherosclerosis? What arteries typically atherosclerose first? What complications does atherosclerosis have in the brain?
Risk factors include smoking, HTN, DM, hyperlipidemia and FH

AA> coronary artery> popliteal artery> carotid artery

Atherosclerotic thrombi can lead to ischemic stroke with subsequent necrosis
Stroke is typically a disease process of advanced age, however, in certain cases, it can occur in younger people. What are some of these circumstances?
Dr. Cordingly says: MOSTLY CARDIAC DEFECTS

Endocarditis
Hypercoagulable states (pregnancy, hormones)
Vascular spasm (migraine)
Vascular malformation (AVM, aneurysm)
Hemoglobinopathy (sickle cell)
Extradural tumors (outside the dura mater) are further categorized into spinal (bone) tumors and intraspinal (btw bone and dura) tumors. What are some examples of each?
Spinal origin, extradural tumors- vertebral metastasis, primary bone tumors

Intraspinal origin, extradural tumors- epidural metastasis
What percent of tumors in the brain are a result of metastasis?
20%
This is a fast growing, most lethal brain tumor. It infilatrates and spreads widely in the brain so surgery cannot remove it. What is it and what can we do?
Glioblastoma multiforme

usually use radiation or chemo (reserved for glioblastoma) --> use carmustine because it can cross BBB
A 7 year old presents with frequent headaches and some bilateral visual field loss. On biopsy, there is evidence of a tumor that looks similar to 'crank case oil'. What is going on?
Craniopharyngioma

Suptratentorial tumor in the sella tursica; can compress the optic chiasma and cause visual field loss
Where are metastatic brain tumors from?
Most metastatic brain tumors are from breast tumors or lung tumors, simply because they are the most common.

Melanoma loves the brain the most.

Prostate CA does NOT metastasize to the brain.
A patient presenting with a cerebellopontine angle tumor will have what deficiencies? Whatis the age of the patient?
Typically will arise as a schwannoma from CN VIII --> auditory loss

ADULTS
Intradural tumors (inside the dura) are further classified into intramedullary (inside the cord) and extramedullary tumors. Please list examples of each.
Intramedullary, intradural tumors- ependymomas, astrocytomas, glioblastomas

Extramedullary, intradural tumors- meningioma, schannomas, neurofibromas
On MRI, a patient is shown to have a tumor that is visualized inside the dura, but outside the cord. What is your tumor differential?
Intradural, extramedullary- meningioma, schwannomas, neurofibromas (neural sheath tumor)
Why would we want to treat a brain tumor with dexamethasone?
Dexamethasone is a corticosteroid --> buys time by shrinking the edema AROUND the tumor
Chemotherapy is usually reserved for which brain tumor?
Glioblastoma multiform

Usually use carmustine because it can cross the BBB
Pediatricians need to be at the forefront of diagnosing mental illnesses. Why?
One half of all lifetime cases of mental illness begin by age 14

Three quarters by age 24
What is the difference between a psychiatric symptom and a psychiatric disorder?

Are more diagnoses made as syndromes or disorders?
Psychiatric symptoms are more isolated events --> can occur in medical conditions, caused my medications, reaction to stress or loss

Psychiatric disorders are a cluster of symptoms that have a characteristic prevalence, onset, and course

***MOST PSYCHIATRIC DIAGNOSES ARE SYNDROMES (no pathognomonic signs)
A patient presents to your clinic in a delusional state. After getting a brief history, you learn that he has not taken his Paxil in four days. Is this a primary or secondary psychiatric disorder?
This is a secondary psychiatric disorder --> d/t a medical condition (he is obviously depressed), medication (withdraw of a med), substance abuse or withdrawl

**A primary psychiatric disroder is when there is NO underlying medical disorder to account for the diagnosis, NOT caused by a medication, NOT caused by substance abuse
Psychiatric illness is a complex entity because EVERYTHING effects it, like...
Perception, cognition, emotion, behavior, environment
What is the DSM-IV (not the individual axis)? What is its use?
Contains a listing of psychiatric disroders, diagnostic codes and criteria for each disorder.

TQ- helpful in diagnosis but does NOT contain info about the etiology or treatment **
What are the Axis Evaluations in the DSM-IV system?
I- clinical disorders (psychiatric- depressive disorder, moderate alcohol abuse)
II- personality disorders, MR,
III- medical conditions
IV- psychosocial and environmental stressors (ie threat of job loss)
In the multiaxial system, where would renal failure fall? Delerium secondary to renal failure?
Renal failure --> III

Delerium secondary to renal failure --> I
Where do the Axis' fall in the biopsychosocial model?
Bio- Axis III- general medical disorders

Psych- Axis I/II

Social- Axis IV
Almost all psychiatric diagnoses are made...

CLINICALLY OR MEDICALLY?
Clinically
Always ask if your patient is suicidal.
Just asking doesn't increase their propensity to do it.
Why do psychiatrists order prolactin levels in their patients?
Prolactin levels increase after a real seizure, not in a pseudoseizure --> narrow diagnosis
What is catatonia?
Catatonia is a syndrome of psychological and motor disturbances

Can include: motor immobility, motor excitement, negativism, mutism, posturing, echolalia, chopraxia, catalepsy (waxy flexability), cataplexy (sudden loss of muscle tone)
On a mental status exam, the patient states that he is depressed. Is he describing mood or affect?
MOOD: sustained emotion as described by the patient.

Affect: expression of emotion as observed by the physician
The normal thought process is...

Circumstantial thought...

Tangential thought...
logical, linear, goal directed

Circumstantial thought is when the person includes many unnecessary details but eventually get to the point

Tangenital thought is when the connections start out apparent, but then never get to point of message
What is the difference betweeen loose associations and flight of ideas?
In loose associations, the patient will jump from subject to subject (schitzophrenia usually)

In flight of idease there is RAPID movement between subjects

**TQ**
Misinterpretation of real stimuli is best described as...
ILLUSIONS

**TQ**
Asking a patient to count backwards from 65 to 49 in threes is doing what?
Testing CONCENTRATION

can they stick with you long enough to complete the task
Asking the patient to name the last five presidents is testing what?
Semantic memory
Constructional ability is tested by what? What are the prerequisites to constructional ability?
copy a 3-D square, draw clock, copy pentagons

Prerequisites- intact vision, motor coordination, strength, praxis, tactils sensation, perceiving overall form (parietal)
What is the first study would you do if someone comes into the ER with complaint of acute headache?
NON CONTRAST HEAD CT
What is the time frame when a hyperacute brain bleed will show up on a CT? What color will it be?
Fresh blood shows up white within 0-3 hours
From where do you measure the midline shift?
Draw a line along the faulx and get a measurement from that to the septum pellucidum.
Where do the majority of epidural hematomas occur?
Frontal temporal area
What are the houndsfield units of bone, water, air, blood and fat?
Water= 0
bone= +1000
air= -1000
blood= 60-80
fat= 0- (-)60
Proton Density MRIs are always done to evaluate...
hips, knees, joints
What three things are black on an MRI?
air, cortical bone, moving blood
White matter is best imaged with a...
FLAIR MRI
How much earlier can MRI detect ischemic injury than a CT?
24-36 hours
What type of hematoma is associated with skull fractures?
Epidural hematoma
A woman comes in with a history of head trauma. On CT you see a bleed contained by sutures (BICONVEX SHAPE). What is this? Is it mostly arterial or venous? Would you check for skull fractures?
Epidural hematoma

90% arterial, 10% venous (66% come from middle meningeal artery)

High association with skull fractures
Suspected child abuse. What hematoma would you be on the lookout for?
Subdural hematoma
Which hematoma is more commonly associated with MVA?

Which hematoma is more associated with falls?
epidural hematoma more common with MVA

subdural hematoma more common with falls
Which hematoma is associated more with venous bleeding? Atrial bleeding?
Venous bleeding- subdural hematoma

Atrial bleeding- epidural hematoma
Match the following:

Acute
Subacute
Chronic
Hyperdense
Isodense
Hypodense
CT density of subdural hematoma

Acute- hyperdense
Subacute- isodense
Chronic- hypodense
What type of edema would be present with a middle cerebral artery infarction d/t infection with necrosis?
Cytotoxic edema --> affects the gray and white matter
What type of edema is associated with tumors of the white matter?
Vasogenic edema
Which is indicative of a persisting confused state? Dementia or delirium?
Dementia
Which artery is typically injured in an epidural hematoma?
The middle meningeal artery runs beneath the pterion. It is vulnerable to injury at this point, where the skull is thin.

**remember, the middle meningeal artery is a branch off of the maxillary artery**
What is the pathology of Alzheimer's Disease?
Widespread cortical atrophy

Amyloid plaques- abnormally phosphorylated tau protein fragments

Neurofibrillary tangles (tangles correlate with degree of severity
What is a PET scan?

How should a normal brain look?

A brain with Alzheimer's?

A brain with Pick's?
PET scan --> radioactive glucose; metabolically active areas show up red, if they are not metabolically active they are blue

Normal brain should have evenly spaced active (red) areas

Alzheimer's- less activity posteriorly (aka more blue posteriorly)

Pick's- less activity anteriorly (aka more blue anteriorly)
What is the basic class of drug we use to slow down the symptomology of Alzheimer's?
cholineresterase inhibitors that are able to cross the BBB
What FDA approved drugs are used in the treatment of mild Alzheimers? Moderate Alzheimers?
Donepezil, galantamine, rivastigmine --> mild/moderate

Memantine --> moderate
What is pathologically characteristic of Pick's Disease? What is Pick's Disease?
Frontotemporal dementia

Will see intracellular Pick bodies --> aggregated Tau proteins
What are the three ways we evaluate tremor? Which is characteristic of Parkinsons?
Max at rest- normally in hands about the pronator/supinator axis (4-6Hz); PARKINSONS

Max at posture holding- hold arms out and they start to tremor, usually about the flexor/extensor axis (8-12Hz)

Max on intention- finger to nose to cerebellum
What are the pathological features of Parkinsons?
Loss of dopaminergic neurons in the SN

Lewy bodies- compositions of a synuclein --> aggregates inhibit proteosome 26
If Alzheimer's and Parkinson's had a baby, what would he be named? How would he present?
Dementia with Lewy Bodies!

Presents as fluctuations in cognitive function with VISUAL hallucinations
What structure is atrophied in Huntington's disease?

What is pathomneumonic of the disease process?
Caudate nucleus

Huntington's Chorea
CJD is a protein folding disease. What proteins are being misfolded?
Abnormal proteins called prions are staying around longer because they have more beta sheets
What is multiple sclerosis?
Autosomal inflammation and demyelination of the CNS --> most of the plaques are in the white matter
A woman comes in with dimming vision over the past several weeks. You prescribe some eye drops and send her on her way. The same woman comes into your office two years later with numbness in her legs. What do you start thinking?
Multiple Sclerosis

Lesions are completely different and are more than 6 months apart
What factors increase the risk of Multiple Sclerosis?
Susceptiblilty in HLA class II gene (DR2)
Late onset of severe childhood infections
Women 20-30
Caucasian
A spinal tap in a patient with Multiple Sclerosis reveals...
Distinct stripes of gamma bands (oligoclonal bands)

Increased protein (IgG)
Which will show up on a CT: concussion or contusion?

What characteristics are associated with each?

Where do contusions normally occur?
Contusions are focal hemorrhages within brain tissue and therefore show up on CT. Concussions are strictly physiologic and do not show up on CT.

Commonly associated with HA, dizziness, irritability, emotionality, poor concentration

Contusions occur at the edge of the brain especially in the anterior temporal and fronal lobes.
How would you different between a subdural and epidural hematoma on a CT? What is the etiology of each?
Subdural hematoma- venous rupture, crescentic lesions (cross suture lines)

Epidural hematoms- artery hemorrhage; secondary to fracture; lens like lesion (does NOT cross sutures)
The Glasgow Coma Scale consists of what information?
Eye opening (1-4)
Motor response (1-6)
Verbal response (1-5)

Coma score ranges from 3-15, 15 being fully conscious

Good for triage decisions, not diagnosis
Which waves are most commonly seen on EEG in a normal brain?
alpha waves (8-13 Hz) in posterior head region
A woman brings her husband to the ER screaming that he had a 'grand mal' seizure. When you ask her to describe the events, she says that...

Is this a partial or generalized seizure?
Initial tonic phase lasting 15 seconds of markedly increased muscle tone

Followed by clonic phase of 120 seconds with rapid jerking

When he came out of it, he was exhausted

Generalized seizure (starts all over brain)
Where do most partial seizures originate?

Where do most generalized seizures originate?
Mesial Temporal Lobe (focal)

All over at the same time
Please compare comlex partial seizures and absence seizures in:

length of seizure
patient
recollection of symptomatology
inheritance pattern
movements
Partial seizure: 2-3 minutes, occur at any age, recall lots of symptoms (odors, deja vu), not inherited, movements look like normal behavior (chewing, picking)

Absence: lasts less than 30 seconds, usually in children or young adults, no symptoms recalled, familial in origin, presents as a blank stare or flutter of eyelids
What is the difference between a hallucination, an illusion and a delusion?
Hallucination- perceptions in the absence of external stimuli (ex. see a light that is not actually present)

Illusion- misinterpretations of actual stimuli (ex. see a light and think it is the sun)

Delusion- false believes that are fimrly maintained in spite of obvious proof to the contrary (CIA is spying on you)
Bizarre and Nonbizarre are subtypes of what? Please explain each.
Bizarre Delusions- clearly implausible, not understandable, and not derived from ordinary life experiences (ex. a guy thinks that someone broke into his apartment, cut him open, stole his organs, replaced them with someone elses and sewed him up without scars)

Nonbizarre Delusions- involve situations that can conceivably occur in real life (ex. being poisoned)
What type of hallucinations occur as one is falling asleep?
hypnagGOgic hallucination occurs as one is GOing to sleep

Hypnopompic occur as one is waking up from sleep
What are positive and negative symptoms?
Positive symptoms are symptoms that are present and should not be: delusions, hallucinations, disorganized speech, disorganized behavior, racing thoughts

Negative symptoms are symptoms that are not there that should be in a normal person: flattened affect, alogia (impoverished speech), avolition (cannot initiate goal directed activities), anhedonia (loss of interest), apathy
What is required in a diagnosis of Schizophrenia?
Periods of psychosis and disturbed behavior with a decline in functioning lasting more than 6 months including 2 of the following:
delusions
hallucinations
disorganized speech
disorganized/catatonic behavior
negative symptoms

Must have a social/occupational dysfunction
Where is schizophrenia most prevalent? (ie. age, gender, location)
M = F, but age of onset is younger in M

Less severe in developing countries

Affects those of lower SES

Genetic factors outweigh environmental factors
What is the difference between schizophrenia and schizophreniform dosorder?
Schizophrenia diagnosis made when symptoms last for more than 6 months. Does require social/occupational function impairment.

Schizophreniform diagnosis made when symptoms last 1-6 months. Does not require impaired social/occupational function.
True Schizophrenia is divided into 5 suptypes. What are they and give a quick explanation of each.
Paranoid- preoccupations with a dellusion

Disorganized- with regarg to speech, behavior an daffect

Catatonic (action without conscious self control, echolalia, echopraxia)

Undifferentiated- elements of all types

Residual- just a behavior disturbance wihtout delusions, hallucinations
There are multiple predictors of outcome of Schizophrenia. What are the good and bad prognostic factors associated with:

onset
duration of symptoms
age at onset
presence/absence of mood
Good:
acute onset, brief duration of symptoms, older age, presence of mood symptoms

Bad: show onset, long duration of symptoms, younger age at onset, mood symptoms absent
What are the time frames associated with:

Schizophrenia
Brief psychotic disorder
Schizophreniform disorder
Schizoaffective disorder
Schizophrenia: sx more than 6 mos.
Brief psychotic disorder: sx less than 1 mo.
Schizophreniform disorder: sx 1-6 mos.
Schizoaffective disorder: at least 2 weeks between symptoms of mood free symptoms
What is delusional disorder?
fixed, persistent, nonbizarre belief system lasting >1 month. functioning otherwise not impaired. self limited.
What type of thought process is associated with schizophrenics?
Loose associations: jumping from subject to subject, idea tenuously connected, never reach the main point
Which axis is depression in?
Axis I
What is the definition of a major depressive episode?
A TWO week period of patient reported depressed mood/anhedonia with:

SIG E CAPS
Sleep disturbance, intrest decreases, guily feelings, energy loss, concentration decreased, appetite/weight changes, psychomotor retardation, suicidal ideations
What is the definition of a manic episode?
Elevated, expansive or irritable mood for at least ONE WEEK with:

DIG FAST
Distractibility, irresponsibility, grandiosity, flight of ideas, agitation, sleepless, talkativeness

Marked impairment in social/occupational functioning that typically requires hospitalization (unlike a hypomanic episode)
What is the definition of a hypomanic episode?
Elevated, expansive or irritable mood for at least FOUR DAYS with:

DIG FAST
Distractability
Irresponsitibity
Grandiosity
Flight of Ideas
Agitation
Sleepless
Talkativeness

does NOT cause marked impairment in social or occupational functioning or require hospitalization (unlike a full blown manac episode)
Which sex is more affected in major depressive disorder? When is the usual onset?
F>M
Rate highest among 25-44 year olds and lowest for those over 65, mean onset in 20s
What is dysthymic disorder?
Patient experiences a depressed mood for over TWO YEARS, but has not met criteria for major depressive disorder

won't go two weeks without symptoms :(
What is the difference between Bipolar I and Bipolar II disorders?
Bipolar I: one MANIC +/- major depressive episode

Bipolar II: one HYPOMANIC plus major depressive episode
What is bipolar disorder?
defined by the presence of at least one MANIC (I) or HYPOMANIC (II) episode. depressive symptoms always occur eventually. patient's mood and functioning usually return to normal inbetween episodes.
What must you have to diagnose bipolar I disorder?
MANIC EPISODE
What is the timeframe for a manic and hypomanic episode?
Manic episodes last more than 1 week

Hypomanic episodes last 4 days
If dysthymic disorder and hypomania had a baby, what would he be named?
Cyclothymic disorder

dysthymia and intermittent hypomanic episodes for 2 or more years
What are the drugs of choice in a tonic clonic seizure? Is a tonic clonic seizure a generalized or partial seizure?
Tonic Clonics are generalized (grand mal)

DOC: valproic acid, carbamazepine, phenytoin
What are the drugs of choice in partial seizures?
DOC: valproic acid, carbamazepine, phenytoin
What are the drugs of choice in an absence seizure?
DOC: ethosuxamide
In generalized seizures, how will the EEGs differ between a nonconvulsive (absence seizure) and a convulsive (tonic clonic)?
In nonconvulsive generalized seizures: 3/second spike and wave EEG

In convulsive seizures: generalized high voltage EEG spikes
What is status epilepticus? How can it be induced? How do we treat this?
Status epilepticus is a continuous state of seizure activity w/o recovery of consciousness

Can be induced by rapid withdraw of antiseizure medications (esp. phenobarbitol, benzodiazepines, phenytoin)

Treat with immediate IV diazepam or lorazepam (benzodiazepine) followed by maintenance dose of phenytoin or phenobarbitol.

Funny, withdraw of the treatments... cause it...
Toxicities include gingival hyperplasia and CV collapse.

What drug is this, it's mechanism of action and what is it used to treat?
Pheynytoin (dilantin)

Slows rate of recovery in Na channels --> decreased firing of neurons

Used to treat all seizures (except absence)
Toxicities include hyperactivity in children and porphyria.

What drug is this, it's mechanism of action and what is it used to treat?
Phenobarbitol

Potentiates GABA inhibition --> decreased firing, elevation of seizure threshold and prevents seizure SPREAD

Alternative treatment to partial and generalized seizures --> childhood hyperactivity have decreased its use
Toxicities include blood dyscrasia and SJS, but NOT urticaria.

What drug is this, it's mechanism of action and what it is used to treat?
Carbamazepine

Slow rate of recovery in Na channels --> decreased firing of neurons

Used in tonic clonic (generalized) seizures and partial seizures
Toxicities include blood dyscrasia, SJS AND urticaria.

What drug is this, it's mechanism of action and what is it used to treat?
Ethosuximide

Decreased conductance of Ca channels --> decreased NT release

Used to treat absence seizures
Toxicities include pancreatitis and hepatitis in kids.

What drug is this, it's mechanism of action and what is it used to treat?
Valproic acid

Blocks Na channel recovery, hyperpolarizes cell via action on K channels and increases GABA --> decreased transmission

So many actions, good for all seizures (except absence)
Can you prescribe a combination of valproic acid, phenobarbital and phenytoin?
Acutely, phenobarbitol inhibits the metabolism of phenytoin, therefore increasing plasma levels of phenytoin. Chronically, phenobarbitol stimulates the metabolism of phenytoin, to decrease levels.

Valproic acid displaces phenytoin from plasma protein binding sites

Valproic acid inhibits metabolism of phenobarbital
A 24 year old female is diagnosed with seizure disorder. You prescribe phenytoin. How do you counsel her on it's use?
It can interfere with oral contraceptives. So don't be a skanky skank.
A 29 year old woman recently found out she was pregnant. She comes to your office asking about her prescription of phenytoin and whether it is harmful to her fetus. You tell her...

Phenobarbital...

Valproate...
Phenytoin- Category D ( use it if there is no other alternative)

Phenobarbital- Category D ( use it if there is no other alternative)

Valproate- Category D ( use it if there is no other alternative); it increases the risk of SPINA BIFIDA
What is lamotrigine?
Adjunct to therapy for partial seizures

Na channel blocker
When should a physician prescribe multiple antiseizure drugs to a patient?
ONLY if more than one seizure type is present or a single drug fails to provide adequate control at near toxic levels
What is ergotamine?
Ergotamine binds to all subtypes of 5HT1/2 receptors --> agonist constriction on cerebral blood vessels --> relief
How do triptans relieve migraines?
5HT 1D/1B receptors constrict large cranial blood vessels, decrease inflammation around sensory nerves and inhibit trigeminal neuronal discharge
Migraine? Drink a Mountain Dew. Why?
no clue. better ask Ryan.
Which triptan agents are used to treat long lasting migraines?
Naratriptan
Frovatriptan
A patient on sumatriptan and fluoxetine is at an increased risk for what?
Sumatriptan --> 5HT agonist

Fluoxetine --> SSRI

Tons of serotonin --> serotonin syndrome --> hyperthermia, muscle rigidity, CV collapse, flushing, diarrhea, seizures

**note- the treatment for seratonin syndrome is CYPROHEPTADINE
What are cluster headaches? How do we treat them?
Cluster headaches are headaches characterized by brief, excruciating, non throbbing pain occuring in a series of attacks; M>F, located around the orbit

use a fast acting triptan (ie. a nasal spray that starts in 15 minutes like sumatriptan or zolmitriptan or a sub Q injection like sumatriptan)
What is the mechanism of a migraine?
release of neuropeptides CGRP, substance P, neurokinin A, serotonin cause vasodilation in the cranial circulation --> dilation of these vessels causes pain
In what populations are triptans contraindicated?
patients with ischemic heart disease, HTN, CAD, angina or basilar migraines
To prevent the occurance of migraines...
B blockers (timolol preferred)
valproate
CCB
wahhhhhhhhhhhh :(
How does treatment with l-dopa improve the symptoms of Parkinson's Disease?
L-dopa is the immediate precursor of dopamine which will cross the BBB --> increased dopamine in the basal ganglia
What are the early and late side effects of l-dopa treatment?
Early: GI irritation, NV, orthostatic hypotension, arrhythmia

Late: tardive dyskinesia, 'on-off syndrome'
What physiologic factors alter the absorption of l-dopa?
rate of gastric emptying
pH of gastric fluids (acidity increases degredation)
dietary protein (the more protein in the diet, the less absorption)
A 67 year old woman with Parkinson's Disease is place on l-dopa therapy. She is currently Centrum Silver, which gives her 150% of her daily recommended value of vitamin B6. Why is this a problem?
Pyrodoxine (B6) increases peripheral conversion of l-dopa to dopamine
What is the mechanism of action of carbidopa? What is it used for?
Carbidopa inhibits the amino acid decarboxylase responsible for converting dopa to dopamine in the periphery, allowing greater amounds of dopa to enter the CNS

It is only available in combination with l-dopa
What is the 'end of dose' phenomenon? How do we treat it?

What is the 'on-off' phenomenon? How do we treat it?
'End of dose' problems are problems that arise when the drug starts wearing off. Entacapone is used with l-dopa to correct this.

'On-off' phenomenon syndrome is characterized by oscillations in preformance involving rapid changes from akinesia to dyskinesia; commonly occurs with l-dopa treatment
What types of drugs are tolacapone and entacapone? How do they work?
COMT inhibitors, thereby increasing the duration of action of l-dopa and dopamine (remember COMT inactivates l-dopa and dopamine)
A patient presents to you with Parkinson's Disease. What algorithm would you use to being their treatment?
Selegiline (MAOB inhibitor) --> dopamine agonist (ropinirole or pramipexole) --> DA + l-dopa --> add COMT --> add all others
This MS drug works like synthetic myelin.
Glitiramer
What are the proposed mechanisms of the following MS treatments?

INF beta
Glitiramer
Mitoxantrone
Natalizumab
Fingolimod
INF- decrease antigen presentation in CNS

Glitiramer- synthetic myelin

Mitoxantrone- suppress immune attack on myelin

Natalizumab- binds to activated lymphocytes and prevents their migration across the BBB

Fingolimod- inhibition of migration of T cells out of lymph nodes
What adverse reaction limits the efficacy of INF B in the treatment of MS?
Antibody formation aginst the INF --> prevents them from producing effect
How are betaseron and rebif administered? What about Avonex? What type of INF are these?
Betaseron (1b) and rebif (1a)- given by alternate day SC injections

Avonex (1a) is given by weekly IM injection
This treatment is used as a monotherapy for MS only once all other treatment options have been exhausted because there is an increased risk of progressive multifocal leukoencephalopathy. What is this drug?
NATALIZUMAB
There is only one drug approved to treat ALS. What is it? How does it work?
Riluzole- blocks Na channels and inhibits glutamate release
What is the most concerning complication of Riluzole therapy? What does Riluzole treat?
Riluzole treats ALS

The most concerning complication of therapy is liver damage
Acetylcholinesterase inhibitors are used to treat some of the symptoms associated with Alzheimer's Disease. Why?
The cognitive effects of the disease are thought to be related to the degeneration of cholinergic neurons in the cortex --> AChEi increase cholinergic activity
Which acetylcholineresterase inhibitors are used in the treatment of Alzheimers?
Donepezil, galantamine, rivastigmine, tacrine

**stop your taCRIne (crying), we'll be DONEpezil with this in galantAMINe (a minute)

this makes no sense, BUT LEARN IT YOU WILL
What is the mechanism of action of memantidine?
NMDA receptor --> blocks glutaminergic overstimulation of NMDA, which can be toxic to neurons which are important in learning and memory
What is the difference between typical and atypical antipsychotic drugs? Where do these drugs act? What symptoms do they treat?
All antipsychotics block D2, but with different affinities.

Typical (chlorpromazine, haloperidol) block D2 the most --> treat positive symptoms

Atypical (clozapine, danzapine) block 5HT and D4 the most--> treat negative symptoms
What neurologic symptoms are associated with antipsychotics?
Acute dystonia- spasms of muscles of the face
Akathisia- can't sit still
Parkinsonism
Neuroleptic malignant syndrome- decrease in BP and catatonia --> stop immediately and treat with gromocryptine or dantrolene
tardive dyskinesia
seizures (especially with clozapine)
A crazy person comes in with PROLONGED QT. What drugs are they on?
Antipsychotics --> especially thioridazine (typical) or ziprasidone (atypical)
What type of antipsychotic drug is clozapine? It is associated with a ton of bad stuff...
Clozapine is an atypical antipsychotic

Associated with a risk of DM, long QT, BMD
What is the biogenic amine theory of mental illness?
Inappropriate amounts of amine NT in body
Fluoxetine and paroxetine are examples of what drug class? What is the mechanism of action of these drugs? What are they used for? What are the most common side effects associated with their therapy?
SSRI (selective serotonin reuptake inhibitor)- acts by blocking the reuptake of serotonin, therefore potentiating the action of 5HT and having little effect on other systems

Treats depression, GAD, OCD, bulemia

Most common side effects are NVD, these are super popular because they act in the CNS only and have no effect on CV or ANS; if used in conjunction with other serotonin saving techniques --> serotonin syndrome
Fluoxetine can be administered daily. Why is this? How long do we have to wait to get our desired result?
Fluoxetine has a half life of 84 hours, which allows a single daily dose

We have to wait about 6-8 weeks for our desired result

Other SSRIs have a shorter half life and therefore can go into depressive withdraw upon cessation
Venlafaxine and duloxetine are examples what drug class? What is the mechanism of action of these drugs? What are they used for? What are the the most common side effects associated with their therapy?
SNRI (serotonin and norepinephrine reuptake inhibitors)

Used in depression, but duloxetine can also be used to treat diabetic peripheral neuropathy and fibromyalgia

NVD still as side effects, but can also drastically increase BP (d/t NE staying around causing vasoconstriction) so watch it!
Bupriopion is an example of what drug class? What is the mechanism of action of these drugs? What are they used for? What are the the most common side effects associated with their therapy?
Atypical antidepressant

Causes presynaptic release of dopamine and NE --> fewer side effects, but does have an increased risk of seizure
Amitriptyline is an example of what drug class? What is the mechanism of action of these drugs? What are they used for? What are the the most common side effects associated with their therapy?
Tricyclic Antidepressants

Main MOA is to block the reuptake of NE and serotonin

They have prominent anticholinergic activity (esp amytriptyline) and can cause sedation, orthostatic hypotension, tachycardia

Overdose is life threatening --> convulsions --> coma --> death, try to treat with physostigmine
Tranylcyromine and phenelzine are examples what drug class? What is the mechanism of action of these drugs? What are they used for? What are the the most common side effects associated with their therapy?
Monoamine Oxidase Inhibitors --> block the metabolism of 5HT and NE in synapse

SE- orthostatic hypotension, dangerous interaction with tyramine, insomnia, tremors, convulsions
A patient with a history of depression presents to the emergency room with a blood pressure of 210/168. His wife states that he met her for lunch at their favorite restaurant, Smoked Cheese, Smoked Fish and Wine Co. Several hours after eating, he started having chest pains and came to the ER. What is going on?
He is probably on an MAOi for depression

Tyramine is found in smoked cheese, smoked fish and wine

When tyramine is ingested, it goes to the liver and is metabolized by MAO, if MAO is inhibited, tyramine can get into the body and cause massive release of NE --> hypertensive crisis
What is the mechanism of action of Lithium? What is the therapeutic range? What if you go above that therapeutic range?
Lithium blocks inositol in nerve cells --> can't make PIP2 --> no cascade of effects

Has a calming effect in a manic patient

Therapeutic range is 0.6-1.25mEq

At 1.6-2.-mEq --> fatique, muscular weakness, ataxia, excessive thirst, excessive urination (acts like an ADH antagonist)

Over 2.0mEq --> impaired consciousness, coma

Must monitor levels VERY CLOSELY
First line drug for depression:

First line drug for Bipolar Disorder: mood stabilizer, depressive episode, manic episode
Depression --> try an SSRI first; if that doesn't work, move on to atypical (bupriopron), tricyclics, MAO, combo, ECT

Bipolar: mood stabilizer in lithium or valproate; depressive episode use lamotrigine (antiepileptic); manic episode use olanzapine
Which drug has the greatest antimuscarinic activity and can cause the most sedation?

Amitriptyline
Desipramine
Fluoxetine

Each of these drugs are from what class?
Amytriptyline- First Generation Tricyclic, STRONGEST ANTICHOLINERGIC ACTIVITY
Despiramine- First Generation Tricycline, still has some anticholinergic activity
Fluoxetine- SSRI
How would bacterial meningitis present?

What lab values would be elevated?
Patient will present with headache, fever, nuchal rigidity, cloudy sensorium, coma death

Gross CSF- purulent inflammation, cloudy CSF, vascular engorgement

Micro- PMN will fill subarachnoid space, will see the causative organism on gram stain

Up to 90,000 neutrophils! decreased glucose
How would viral meningitis present?
They don't look super sick, self limiting

100-1,000 lymphocytes! normal glucose

Gross CSF- mild inflammation and brain swelling

Micro- very little infiltrate
What is the most concerning long term sequelae of bacterial meningitis (sp. the leptomeninges)?
HYDROCEPHALUS and leptomeningeal fibrosis

plugging of circulation of CSF --> increased pressure
Fungal meningoencephalitis is most commonly seen in what type of patient?
Immunocompromised (AIDS, old people)!

LUNG TO BLOOD TO BRAIN is the typical spread
Disseminated infections are commonly seen in immunocompromised patients. In an immunocompromised patient with meningitis, what can we expect?
Fungal meningoencephalitis is common in immunocompromised patients

Parasitic meningoencephalitis --> toxoplasmosis is the most common concern because of involvement with AIDS (up to 30%)
What is the most common causative agent of bacterial meningitis in the following age groups?

Neonates to 3 months
3 months to 10 years
10 years to 19 years
20 years to 60 years
Elderly
Neonate to 3 months: group B strepptococcus

3 months to 10 years: N. meningitidis

10 years to 19 years: N meningitidis

20 years to 60 years: 50:50 Neisseria to Pneumo

Elderly: Streptococcus pneumoniae
What is the most common causitive agent of meningitis in the elderly? Describe this organism. Catalase? Fermenter? Morphology? Hemolysis?
Streptococcus pneumoniae

Gram positive, lancet shaped diplococci in chains, catalase negative, ferment sugars --> lactic acid --> low pH, Alpha Hemolysis
What is the most common causitive agent of meningitis in neonates? Describe this organism. Catalase? Hemolysis? Morphology? Capsule?
Gram positive cocci in chains, catalase negative, beta hemolysis, **sialic acid capsule**
What is the most common causitive agent of meningitis in adolescents 10-19 years old? Morphology? Oxidase?
Neisseria meningitidis- gram negative, coffee bean shaped diplococci, oxidase positive
What virulence factors are associated with N.meningitidis?
pili!
capsular polysaccharide (this is different from n. gonorrhea)
outer membran proteins
endotoxin (all G- have this)
Hemophilus influenzae has been known to cause meningitis. What is its morphology?

Why is it no longer really an issue?
Haemophilu influenzae is a small, gram negative, pleomorphic, fastidious rod

hemophilus (loves heme)- grows on X factor (heme) and V factor (NAD)

After the development of the HIb vaccine, it was the leading cause of meningitis in young kids! Still be on the lookout in kids from Europe who never got the Hib vaccine.
Listeria can often cause infection in the elderly and the immunocompromised. Morphology?

What would tip us off that the meningitis is caused by listeria?
Gram postive rods with a distinctive TUMBLING motion, beta hemolytic

associated with food poisoning --> it can survive the refridgerated temperatures.

Hx of ingestion of cold cuts **
How does Neisseria meningitidis typically enter the body?
Colonization of the oropharynx --> enters the blood stream through the mucous membranes --> resist killing primarily by capsule formation --> penetrates the BBB at the choroid plexus --> inflammation spilling into the CNS
Which cytokines are responsible for the inflammatory damage due to Neisseria meningiditis invasion?

How can this initial infection lead to headache?
IL1 and TNF

Clinical symptoms d/t inflammatory response to meningeal invasion --> fluid becomes thick --> blockage of foramina and increase in CSF pressure --> headache and nausea --> neurological defecits caused by decrease in cerebral cortical blood flow
A 12 year old patient presents with a severe headache, stiff neck, rash and photophobia. You begin to suspect bacterial meningitis. What is your immediate action?
INITIATE ANTIMICROBIAL THERAPY PRIOR TO IMAGING STUDIES

**remember, if they have severely increased pressure, spinal taps are contraindicated
How many tubes of CSF should you collect for analysis of potential meningitis? How would you differentiate between viral and bacterial meningitis based on the CSF? (ie cell type and number, glucose)
Three or four tubes should be collected

Bacterial meningitis- over 1000 cells/mL, 50% PMN, glucose levels are decreased (bacteria use glucose for energy)

Viral meningitis- 10-1000 cells/mL, lymphocytes predominate, glucose levels ok
Which virulence factor is common to all meningitis causing bacteria?

Which other non meningitis bacteria share this factor? How do you test for it?
CAPSULES (sialic acid)

Kapsules Sheild SHiN --> Klebsiella, Salmonella, Streptococcu pneumoniae, Hemophilus influenza, Neisseria meningitis

postive Quelling reaction
In HIV patients, what are the most common causative agents of meningitis?
cryptococcus, CMV, toxoplasmosis (brain abscess)
What is the DOC for bacterial meningitis?
vancomycin + cefptaxime or ceftriaxone + dexamethasone

Antibiotic must be able to penetrate BBB --> but with so much inflammation, it is easy to cross the BBB
What is the difference between a conjugate vaccine and a polysaccharide vaccine?

Which type is the Hib vaccine?
A conjugate vaccine is a T cell dependent antibody response that utilizes the protein antigen to induce memory production of IgG; BOOSTER!

A polysaccharide vaccine is a T cell independent antibody response that utilizes polysaccharide antigens to produce IgM; NO MEMORY, little boosting

The Hib vaccine is a conjugate vaccine.
Surgery can be responsible for introducing which organism into the brain, resulting in brain abscess?
staph aureus