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261 Cards in this Set

  • Front
  • Back
What are the main features of isolated syndrome of the first presentation of MS?
Optic neuritis
Transverse myelitis
Brainstem syndrome
What is the clinical presentation of transverse myelitis?
Disthesia
Paraplegia
How does brainstem syndrome present?
Double vision
Lack of balance
Incoordination
Name three variant forms of MS
Marburg's variant - severe axonal loss
Balo's concentric Sclerosis
Neuromyelitis optica
How can diffuse lesions seen on MRI be diagnosed as MS
Temporal dispersion
Spatial dispersion
of demyelinating disease activity.
ADEM
Acute Disseminated Encephalomyelytis
Onset of ADEM
2-3 weeks after a viral infection
ADEM is monophasic:
Happens once, after the insult and has an endpoint. all the lesions are of the same age.
Dawson's finger:
Seen with multiple Sclerosis, a plaque which is perpendicular to the lateral ventricle.
True or False:
MS is both a demyelinating disease and one that causes axonal injury.
True
What does multiple in MS mean
Lesions are multiple in space and happen at different (multiple) time.
Symptoms of X-linked adrenoleukodystrophy in children (age 4-8)
ADHD like
Progressive impaired cognition
Behavior,
Loss in vision and hearing
*** loss of milestones ***
Symptoms of X-linked adults:
More like primary progessive MS
How do you diagnose X-ALD?
Mostly males (x -linked)
MRI - abnormal
Increased VLFCA - Very Long Fatty Chain Acids
Symptoms of subacute combined degeneration in B12 deficiency
Weakness
Abnormal sensation
Mental problems
Vision difficulties
What nn does peripheral neuropathy involve?
Sensory
Motor
Both
How does peripheral neuropathy present, sign:
Reduced or absent muscle reflexes.
Distal - proximal weakness
Atrophy
Reduced sensation
List Five peripheral neuropathy patterns:
Distal symmetric neuropathy
Mononeuropathy
Multiple mononeuropathy
Autonomic neuropathies
Small Fiber neuropathy
Distal symmetric neuropathy -
Etiologies
Diabetes and toxic neuropathies (chemo and toxic alchohol use)
Mononeuropathy - Etiologies
One nn affected
Carpal tunnel syndrome (Median NN pinched - weak hand)
Ulnar neuropathy - numb and tingling of medial 2 fingers
Perineal neuropathy @ fibular head (Foot drop)
Multiple mononeuropathy
(Assymetric, more than one nn, possible nn infarction)
Inflammation with autoimmune disease eg. LUPUS, Polyateritis nodosa
Clinical Features Autonomic neuropathies:
Dysautonomia eg. urinary retention, erectile dysfunction, postural HTN.
Autonomic neuropathies:

***ETIOLOGIES ***
Diabetes
***AMYLOIDOSIS ***
Small Fiber neuropathy: Symptoms
Tingling/ Burning/ Pain sensation.
Small Fiber neuropathy: Signs
Abnormal neurological exam but EMG/NCS normal (examine large fibers)
Small Fiber neuropathy: Dx
Count small nn fibers (less) on epidermal nerve fiber assessment by skin biopsy.
What is Charcot-Marie Tooth (CMT) disease:
Most common inherited neurological disorder
Can be AD (More), AR, X-linked.
Affects peripheral myelin - uniform demyelination
What are the patterns of peripheral nn damage?
Neuronal damage (ALS, Sjorgen's disease, Anti-HU paraneoplastic disease)
Axonal inury (Wallerian degen and atropy of muscles)
Demyelinating disease (Guillain-Barre & CIDP)
What is Guillian-Barre syndrome?
Aquired autoimmune disorder
Recent URI or recent vaccine
First tingling and weakenss of legs --> weak arms
May not be able to breath with time.
Arreflexia.
Usually transient, could revert to normal in a few weeks.
Normal sensory function.
What tests would you do if suspect Guillan-Barre syndrome.
*** MUI IMPORTANTE ***
EMG MAY BE NORMAL IMMEDIATELY AFTER ONSET, DON'T DO THIS.EMG WOULD BE NORMAL EARLY.
TAP CSF - CHECK FOR INCR. PROTEIN CONTENT WITH NORMAL CELLULARITY.
Rx of Guillain Barre syndrome:
DO NOT GIVE STEROIDS - May deteriorate
Give IV Immunoglobulins
Plasma exchange - get rid of the antibodies attacking the patients nerves.
What is CIDP (Chronic Inflammatory Demyelinating Polyradiculoneuropathy)?
Chronic variety of Guillain -Barre
Repeated attacks of demyelination
slower onset > 8 wks
Elevated CSF protein
EMG - may see acquired demyelination - conduction block.
Two markers for acquired demyelination
Conduction block
Temporal dispersion
Rx of CIDP syndrome:
Steroids
IV Immunoglobulins
Plasma exchange
What is Parsonage-Turner Syndrome (Aka Brachial plexus neuritis)?
Signs and symptoms
Preceeding hx of vaccination, infection, diabetes, Sjorgens
Burning pain in arm
Weakness
numbness
Atrophy of nerve may dvp.
Weakness of muscles innervated by anterior interosseous (branch of median nn)
Weak flexor pollicus longus & Flexor digitorum profundus
Name three motor neuron diseases:
ALS
Spinal Muscular atrophy
Spinal Bulbar Muscular atrophy (kennedy disease)
Which motor neuron disease is X-linked, have CAG repeats with anticipation?
Spinal Bulbar Muscular atrophy (kennedy disease)
Which motor neuron disease is Autosomal recessive and has mutation in ***chromosome 5Q ***?
*** MUI IMPORTANTE ***
Spinal Muscular Atrophy (Presents as floppy infant"
What is common about the sensory system in motor neuron diseases?
Have normal sensory
(3) NMJ disorders
Myasthenia Gravis
Eaton-Lambert Syndrome
Congenital myasthenia
Are there sensory symptoms associated with NMJ?
NO, NMJ between motor nn and muscle.
What is Myasthenia Gravis?
Acquired
Autoimmune
Weakness (Ocular - eyelid ptosis [ Binocular diplopia ...symptoms flactuate], limb weakness and bulbar fatigue [trouble swallowing, chewing, breathing]
What is the pathology of Myasthenia Gravis?
Antibodies againts Ach or Muscle Specific Kinase (MuSK - against tyrosine kinase), simplifaction of postsynaptic membrane.
What are the symptoms of Ocular MG?
Eyelid ptosis/ diplopia without generalized weakness.
Diagnosis of Myasthenia Gravis?
Flactuating weakness pattern, usually more proximal.
Check receptor ab.
NCS - repetitive nn stimulation and observe ampl of signal. Decr. response suggests affect postsynaptic end.
Tensillon test
Ice pack test - cooling eye may resolve ptosis, help eye muscle depolarize synchronously.
Describe Tensillon test that is used to diagnose MG.
Tensillon test - Achesterase inh, inh break down of Ach, prolonging Ach, help patient sustain muscle contraction.
What tumors are associated with MG?
Thymic tumors (10-15%), diagnose by CAT scan. Removing tumor can improve response of disease to treatment.
How is MG treated?
AChesterase inhibitor - treat symptoms
Immunosuppresant drugs:
Steroids, steroid sparing agents, IVIg, plasma exchange
What is the difference between neonatal MG and congenital MG disorders?
The latter last longer than 12 weeks and are due to defect in NMJ. The neonatal MG is due to antibodies present due to having a mother that has MG. Usually lasts 12 wekks.
Vast majority of Congenital myasthenia gravis disorders are inherited in an:
*** MUI IMPORTANTE ***
AUTOSOMAL RECESSIVE FASHION
What is the majot difference between the pathology of Lambert Eaton myasthenic syndrome (LEMS) and MG?
LEMS - acquired autoimmune disease that affects the presynaptic terminal.
MG - acquired autoimmune disease that affects the postsynaptic terminal.
What diseases are associated with LEMS?
Small cell lung cancer
Lymphomas
Why do LEMS improve with exercise or electrical stimulation in lab?
Antibodies to presynaptic membranes and interferes with the release of Ach vessicles. As use muscle more, allow more Ach to be released and thus available and hence less symptoms.
Why do we see upregulation of postsynaptic folds with LEMS?
Lack of enough Ach leads to upregulation of receptors on postsynaptic memrbane.
What is the difference between response of MG to exercise and response of LEMS to exercise?
*** MUI IMPORTANTE ***
Incremental response with LEMS and decremental response with MG.
Pathology - what membrane is involved in botulism?
Pre-synaptic mebrane - C. botulinum (neurotoxin).
Symptoms and signs of botulism?
Weakness
EOM involved
Pupils spared
Constipation
What are myopathies?
Disorder that affects muscle
Affects proximal more than distal.
spillage of muscle enzymes - Aldolase, lactate dehydrogenase, CPK
Inherited or acquired.
Signs and symtpoms of myopathies:
Weak
Muscle cramps
Exercise induced pain
Myoglobinuria - due to break down of muscles
No sensory symptoms
Inherited myopathies
Muscular dystrophy
Metabolic myopathies
Congenital myopathies - present with floppy baby syndrome
Mitochondrial myopathies
Acquired myopathies
Inflammatory myopathies
Infectious myopathies
Toxic myopathies
Diagnostic tests for myopathies:
Needle EMG
Char small motor unit potentials - short duration and short amplitude
Early recruitment - due to weak muscles.
NERVE CONDUCTION IS NORMAL
Elevations in muscle enzymes and may have elevations of liver enzymes: CK, Lactate, aldolase, AST, ALT
Muscle biopsies
Differential Dx of muscle myopathies:
Muscle myopathy
Muscle trauma
Exercise
Increase muscle mass
Variation due to ethinicity & gender
What are muscular dystrophies?
Hereditary
Progressive with time
Degenerative
Variable onset in intensity of disease.
Give examples of muscular dystrophies:
Duchenne (X-linked, dystrophin)
Becker (X-linked, dystrophin)
Limb-girdle (AD, AR, X-linked - affect more hip)
Emery-Dreifuss (Contracture of arm muscles, lots of cardiac disease)
Facioscapulohumeral
Myotonic dystrophy (Difficulty relaxing muscles)
Oculopharyngeal muscular dystrophy (mitochondrial diseases)
Give examples of inflammatory myopathies:
EMG - see denervation
Polymyositis
Dermatomyositis - also rashes on skin usually elbows
Inclusion body myositis - affects older patients. No response to treatment
Which two inflammatory myosities present in two peaks?
Polymyositis
Dermatomyositis - 2nd peak usually associated with cancer.
How would you evaluate a possible toxic myopathy caused by Lipid lowering agents?
*** MUI IMPORTANTE ***
Check CK levels, DO NOT CHECK EMG, WOULD BE NORMAL.
Past medical Hx associated with mitochondrial myopathy:
Diabetes mellitus
Short stature
Sz
Deafness
Three syndromes associated with mitochondrial myopathies:
*** MUI IMPORTANTE ***
Myoclonic Epilepsy with Ragged Red Fibers (MERRF)
Mitochondrial Encephalomyopathy, Lactic Acidosis, Stroke (MELAS)
Mitochondrial, Neurogastrointestinal Encephalopathy Syndrome (MNGIE)
MRI of Mitochondrial Encephalomyopathy, Lactic Acidosis, Stroke (MELAS)?
*** MUI IMPORTANTE ***
Look like they have stroke but resolves in days.
What are periodic paralysis?
*** MUI IMPORTANTE ***
Muscle channelopathies
Occur in episodic attacks
Cause transient weakness
Etiology of periodic paralysis?
*** MUI IMPORTANTE ***
**LARGE CARBOHYRDATE MEALS **
Rigorous exrecise
Emotional stress
Change in serum potassium levels
Two flavours of periodic paralysis:
Hyperkalemic - Ca+ channelopathy, hrs - days
Hypokalemic - Na+ channelopathy, min - hrs
How would you treat hyperkalemic periodic paralysis?
*** MUI IMPORTANTE ***
ACETAZOLOMIDE
TRUE OR FALSE
Romenberg is a test of cerebellar function
False:
Romenberg tests proprioception.
What are Lewy bodies?
*** MUI IMPORTANTE ***
Cytoplasmic inclusions of alpha-synuclein, seen in Parkinsons Disease.
What is the difference between Levodopa and Dopamine?
Levodopa can cross the BBB whereas Dopamine cannot.
Complications of Levodopa therapy?
Wild movements
Dyskinesia
Hallucinations
Nausea
Orthostatic hypotension
Name some causes of secondary parkinsons:
Neuroleptics
Reglan & Metaclopromide - meds. for GI probs.
Cerebrovascular stroke
MPTP
Dementia Pugilistica - Muhammad Ali
The four cardinal clinical features of Parkinsons:
*** MUI IMPORTANTE ***
Bradykinesia
Resting tremor
Cogwheel rigidity
Postural instability
First line treatment of PD:
*** MUI IMPORTANTE ***
Carbidopa/Levodopa
List 4 Parkinsons plus syndromes:
*** MUI IMPORTANTE ***
Progressive Supranuclear palsy (PSP)
Dementia with Lewy Bodies (DLB)
Multiple System Atrophy(MSA)
Corticobasal Degeneration (CBD)
Progressive Supranuclear Palsy (PSP)
*** MUI IMPORTANTE ***
Gaze palsy, **Fall early on, Nucchal rigidity, Speech disorder.
What % of strokes are due to Ischemia?
80%
Define lacunar stroke
Lake - very small stroke from basilar artery branch occlusion.
Stroke warning signs:
Sudden weakness of face, arm, leg on one side of body
Sudden confusion, trouble speaking
Sudden trouble walking, dizzy, lack of balance or co-ordination
Severe headaches - Thunderslap- with no known cause
Define TIA
Temporary focal neurological deficit of brain related to ischemia or brain or retina < 24hrs. Symptoms clear up after 1hr.
What part of the brain is improtant for understanding language?
Wernickes area
What part of the brain is speech area?
Broca's area
What artery is involved in patient with: Right hemiparesis, Right sensory loss, Right homonymous hemianopia, Aphasia - (global, Broca's, Wernicke's),Dysarthria (sound drunk), Alexia, Acalculia.
Left Middle Cerebral Artery
Define Broca's Aphasia
Can comprehend language but their speech is broken.
Define Wernicke's Aphasia
Fluent speech but difficulty in understanding.
Define Alexia
Inability to read words/ text
What symptoms might differentiate a stroke on the right side from left side?
Neglect of left side, Anosognosia (don't recognise what's wrong with them), Loss of prosody of speech, Flat affect, Extinction, Apraxia
Define Extinction as a sign for R. MCA stroke.
Touch both hands of patient with Right MCA stroke, can only feel touch on the right side
Define apraxia as a sign for R. MCA stroke.
Patients does not know to something which they formerly knew but now they don't.
Dressing apraxia
Constructional apraxia
Define Topographic memory deficit as a sign for R. MCA stroke
Lost in farmiliar sorroundings
What are the three main clinical features of Posterior Cerebral Artery occlusion:
R/L homonymous hemianopia (contralateral of deficit)
Hemi-ataxia
Color-anomia : unable to id colors
Prospognosia - if involves parietal lobe- can't recognize faces.
A patient comes in presenting with: Decr. consciousness, contralateral hemiparesis, dysarthria, hoarseness, vertigo, nausea, vomit, hearing loss:
Brainstem stroke
4 nonmodifiable risk factors for stroke:
Family history
Age
Race
Sex - Males more than females
Modifiable risk factors for stroke
Htn
Diabetes
Cigarrete smoking
Hyperlipidemia
Obesity
Cardiovascular problems
ATRIAL FIBRILLATION
Alchohol
History of previous stroke
Carotid stenosis
How do you diagnose a patient you suspect to have a stroke?
*** MUI IMPORTANTE ***
CT scan - to determine if BLOOD IS INVOLVED (ischemic or hemorrhagic?)
MRI -If CT scan not clear, get more information
Echocardiogram - function of heart
Arteriography - vessel function
list three etiology classes that are involved in ischemic stroke:
Cardiac manifestations
Large vessel disease
Small vessel disease
Hematological disorder
How do you treat stroke acutely?
If stroke is within 3hrs, tPA can be given; Don't give to those with TIA or likely to hemorrahge.
Aspirin - If given within 48hrs of time of onset. Give this if can't get tPA
How are stroke patients surgically managed?
Carotid endarterectomy: Do to prevent stroke, if really narrowed artery.
Hemicraneotomy: Stroke patients with swollen brain to decrease mass effect and herniation.
Preventive medications for stroke:
Antiplatelet agents (Aspirin, Clopidogrel,Anticoagulation - warfarin/coumadin)
Define Sz
Sudden rythmic change in electrical activity usually accompanied by change in behavior
Difference betw. simple partial and Complex partial Sz.
Both have auras, but complex partial has loss in awareness whereas simple partial does not.
Who is an epileptic?
Had 2 or more unprovoked Sz
EEG abnormalities in an epileptic:
Spikes and sharp waves
What is the most common cause of medically refractory symptomatic epilepsy:
Hippocampal sclerosis - CA1, CA3, CA4 damaged, CA2 spared.
What is the most common cause of medically generalized symptomatic epilepsy:
Global anoxia and tuberous sclerosis
Name the epilepsy syndrome:
Onset: 4-8yrs old
EEG: 3Hz spike and wave
Rare GTC
Respond well to meds
Childhood absence Sz
Name the epilepsy syndrome:
Onset: 12-18 old
EEG: 4-4.5Hz spike and wave
GTC possible
Sz in morning
Respond well to meds
Juvenile Mycolonic Epilepsy
Name the epilepsy syndrome:
EEG: Charecharestic
Multiple Sz types
Mental Retardation
Not treatable
Lennox-Gastaut syndrome
Name the epilepsy syndrome:
Onset: 5-9yrs old
Sz: focal motor - unilateral facial twitching.
GTC - only at night
Normal MRI
Only idiopathic partial epilepsy
No treatment necessary
Benign Rolandic
Name the epilepsy syndrome:
Onset: childhood or adolescence
Hx: predisposing hit - complex febrile Sz
Origin: Hippocampus / amygdala
few GTC
Not medically controlled
EEG: Focal temporal spikes
Aura
Automatisms
Mesial Temporal Lobe epilepsy
Name the epilepsy syndrome:
SZ - at night mostly
Bizarre and complex automatisms
Fencers posture
May spread to temporal lobe - MTLE
Frontal Lobe Epilepsy
Name the epilepsy syndrome:Presents simply with GTC
Neocortical epilepsy
This Sz last for a min like clockwork:
GTC
The Sz that lasts the longest: 2 min
Focal
List 4 types of generalaized Sz
GTC
Myoclonic
Absence (typical and atypical)
Atonic
List 2 types of Focal SZ
Simple partial
Complex partial
Name two drugs that can provoke Sz
Clozapine and cyclosporine
Which epipleptic syndrome doesn't need treatment
BRE
Most common aura associated with MTLE
Rising epigastric sensation
Difference between patients energy level after frontal lobe sz as compared to temporal lobe sz
Frontal - feel fine
Temporal - tired
Which epipleptic syndrome respond to treatment?
CAE
JME
Which epipleptic syndrome do not respond to treatment?
Lennox Gastaut syndrome
MTLE
What is the treatment of choice for MTLE?
Surgery
What is the new std of care of Glioblastoma multiforme?
Temozolamide with radiation therapy
4 main cancers associated with brain metastases
Lung
Breast
Melanoma
Colon
Symptoms that a patient with brain metastases may present with:
Headache
Seizures - 10%
Cranial palsies
Focal weakness
When would you resect a single brain metastasic lesion?
If patient has KPS>70 and is funtionally independent.
If patient has KPS<70, do it for palliation.
What does this patient have?
Unilateral headache
Moderate
Pulsating
Photophobia and phonophobia
Has has this before, no other disorder
Migraine without aura
What does this patient have?
Bilateral pain
Mild- moderate
No aggravated by physical activity
No other symptoms excpet slight nausea
Non-pulsating
No other organic disease
5 previous attacks
Each attack lasts 30min to 7 days
Tension-type headache
Patient has severe headache in V2 V3 area of trigeminal nn distribution on the face.
Trigeminal neuralgia
What does this patient have?
Severe unilateral pai lasting 15 min to 180 min.
Ipsilateral nasal congestion.
Has headache every other day
Had 6 attacks
SMOKER
Cluster headache
What are the red flags that might indicate an important secondary headache?
*** MUI IMPORTANTE ***
Systemic symtoms
Secondary Risk factors
Neurologic symptoms
Onset: sudden, split second
Older
Previous headache
A patient with chronic migraine complicated by overuse of medication has:
Rebound headaches
What kind of headache?
Migraine preceeded by one neurological aura
Migraine with Aura
Also know as a suicide headache:
Chronic cluster headache
What are the most common neurodegenerative diseases that cause dementia?
Alzheimers - 70-80%
Lewy body disease - 10-15%
Frontal Temporal Degeneration - 5-10%
Define dementia
Progressive disturbance in cognition and can be diagnosed by history and exam - clinically
Difference between delirium and dementia
Delirium: Loss of attention and hallucination over a period of days and usually due to metabolic insult. Reversible.
Dementia: Focal Loss in cognitive abilities over a period of years. Usually have brain lesion and is not reversible.
What is the basic pathway in pathogenesis of neurodegen. diseases?
Failed biochem pathway --> accumulation of junk --> neuronal dysfunction and death.
What are the different parts of papz circuit
Hippocampus--> Fornix --> mammilary bodies --> Anterior thalamus --> Cingulate
When is an EEG used in diagnosing Brain pathology?
When suspect epileptic Sz.
Altered levels of consciousness or coma
What is Epileptiform activity seen on EEG?
Abnormal brain activity which predisposes a patient for epilepsy. This activity is like a short circuit, presents as a sharp wave.
You are looking for epilepsy and obtain a normal EEG. What are your conclusions:
Cannot rule out epilepsy, may not have picked up activity
Nerve conduction studies can be done to asses for:
Peripheral neuropathy
Charcot-Marie tooth disease
Acute demyelinating neuropathy
EMG studies can be done to asses for:
ALY
Polymyositis
Muscular dystrophy
What are you testing when carrying out evoked potentials?
Connection btw peripheral nn and CNS. Combines NCS and EEG. Used in Multiple sclerosis, myelopathy and conversion disorder.
Describe a digital subtraction angiography
Catheter --> femoral artery -->brain artery --> inject contrast --> look for abnormality --> treat with endovascular therapy
When are CAT scans a preferable technique when assesing the brain?
Acute and subacute hemorrhages - bright on scan
Emergencies - takes abt 10 min.
Spinal cord imaging - bony images
CAT angiography - like X-ray only this is via veins and can be used for non-interventional procedures.
How would you treat a post Lumbar punture headache?
Bedrest, fluids, caffeine
If that fails, may need a blood patch
When are MRI's a preferable technique when assesing the brain?
Able to discern the structure of the brain.
Allows Dx of:
small Strokes (diffusional MRI)
MS
Define the term: Delusion
A false and fixed idiosyncratic belief
Define the term: Illusion
Misperception of real external stimuli
Define the term: Hallucination
Sensory perception that has compelling sense of a true perception but occurs without external stimuli.
Describe the pentaxial system that pyschiatrists use in assesing a patient:
Axis I - Clinical psychiatric disordres
AxisII - Personality disorders and mental retardation
AxisIII - non-pyschiatric disorders
Axis IV - Acting stressors
Axis V - Global assesment of funtion.
What are the diagnostic criteria of a panic disorder without agoraphobia
Recurrent unexpected panic attacks and followed by atleast one month of:
- Fear of attack -
- Change of behavior related to attacks -
-worry abt consequences of attack-

Absence of agoraphobia
No other medical or mental disorder 18 -35 yrs old
When do we see onset of panick attacks?
18 - 35yrs old
How do you work up what looks like a panic attack?
Hx - medical and pysch
PE and NE
Mental status exam
Medication hx
Drugs?
EKG if >40
CBC
Thyroid function test
What are the diagnostic criteria of a panic attack
Intense fear with four or more symptoms associated with increase adrenaline (abrupt and peak in 10min.)
palpitations
sweat
trembling
Fear of dying
Agoraphobia
Fear of being in places where help might not be available. 2.5 - 6% prevalence
How would you treat panic disorder?
SSRI - First line, *lower *concentration than used for depression (Paroxetine, Sertraline, Escitalopram)
TCA's - (Imipramine, Cloripramine)
BZD - (Clonazepam)
MAOI's - (Phenelzine)
Cognitive behavioral therapy - desensitization and behavioral training
How would you treat social phobia?
B-Blockers
Generalized phobia - SSRI's and MAOI's
What makes a panic attack a panic disorder?
Recurrent unpexpected panic disorder
Name the different anxiety disorders:
Panic disorder
Social phobia
Specific phobia
OCD
Post Traumatic Stress Disorder
Acute Stress Disorder
Generalized Anxiety disorder
Anxiety disorder due to a general medical condition
Substance-induced anxiety disorder.
How would you treat OCD?
SSRI's - Dose higher than that used to treat depression.
Paroxetine
Fluoxetine
Sertraline
Fluvoxamine
TCA - Clomipramine
Behavior therapy
BZD's - not very useful in treating OCD
What disorder doe this individual have:
He has had this symptoms for >1 month:
BOTH: Has experienced lifethreatening event AND This involved intense fear
Re-experience thru dreams/ flashbacks
Avoidance of stimuli associated with trauma
Increased arousal - INSOMNIA, ANGER ...
Post Traumatic Stress Disorder
How would you treat PTSD?
First line: SSRI - Sertraline
Mood stabilizer - Buspirone

*2nd line*
Beta-blocker - propanolol
Atypical antipsychotics
How would you treat Generalized Anxiety Disorder?
First line:SSRI - Venlafaxine
Buspirone - also first line
BZD - not very useful
Congitive behavioral therapy
Diagnostic criteria for GAD
For more than **6 months** patient:
Worries too much
Can't control their anxiety
Has at least three of the following
-Restless
-Tired easily
-Dificulty concentrating
-Irritable
-Muscle tension
-Sleep distubance
DOES ANTICIPATE A PANIC ATTACK
Is causing them sig. distress
Not using drugs or with any other medical condition
What is the lifetime prevalence of PTSD?
10%
In patients with GAD, does their worry tend to serve a defensive function?
Yes, worry about superficial things so that one doesn't have to deal with the true concern.
The cell bodies are confined primarily to the locus ceruleus, name the NT
NE
Benzodiazepines enhance effects at its receptors;name the NT
GABA
The cell bodies are localized primarily within the raphe nuclei;name the NT
Serotonin
What disorder is associated with Isolation, undoing, and reaction formation
OCD
List (5) mood disorders:
Depressive disorders
Bipolar disorders
Adjustment disorder with depressive mood
Aubstance-induced mood disorder
Modo disorder due to medical condition
What mood disorder does this individual have?
@least 2 wks of persistent mood, cognitive & behavioral symptoms
>5 of the following symptoms nearly all the day, nearly all the time
**Low mood
**Anhedonia- decr. interest in activities
**Weight loss/ gain
**insomnia/hypersomnia
** Pyschomotor agitation or retardation
**Fatigue or low energy
**Feel worthless or guilty
**Indecisive, impared decisions or memory
**recurr. thots of death or suicide
Major Depressive disorder
List (3) depressive disorders:
Major depressive disorder
Dysthymia
Depressive disorder NOS
Patient presents with Chronic depression, has had it for more than 2 years. The patient has not been without symptoms for more than 2 months during the 2 yrs. Milder than major depressive disorder.
Dysthymia
What mood disorder does this individual have?
@least 1 wk *persistent* elevated, expansive or irritable >3 of 7 all in same week:
Grandiosity
Decreased NEED for Sleep
Pressured speech
Racing thoughts
Distractability
Pyschomotor agitation or excessive activity
Excessive indulgence in pleasurable with poor judgement.
Manic episode
What is this person suffering from:
Mild form of mani <4 days
NO PYSCHOSIS
No major impairement of function
Hypomanic episode
This mood state is a poor prognosis of bipolar, patient has mania and depression at same time and terrible "bouts" of pyschosis
Mixed episode
Describe a Bipolar II disorder
One or more hypomanic episode
and
Depressive episode
HAS NEVER HAD AN EPISODE OF MANIA
Describe a cyclothymic disorder
Chronic depression (milder than major)
Alternating with hypomania
for 2 years,
Patient should not be without symptoms for more than 2 months during the 2 yr period
Give examples of substances that can induce mood disorder

*** MUI IMPORTANTE ***
Steroids - Mania
Oral contraceptives - depression
Cocaine - induced mania
Epidemeology of Bipolar I disorder:
What is the point prevalence?
1-2%
Males:Females
Epidemeology of Bipolar II disorder:
What is the point prevalence?
0.5%
More common in females
Epidemeology of Major depressive disorder:
What is the point prevalence?
5-9% Female
2-4% male
No sex diff in childhood

Lifetime prevalence: 20-25% F
7-12%M
Epidemeology of Dysthymic:
What is the lifetime prevalence?
6%
3F:1M
Which of the two has the greatest degree of genetic predisposition?
Bipolar disorder
What functions of the body are affected by the monoamines involved in Bipolar disorder and major depressive disorder?
Arousal, Sleep patterns, motivation, aggression, pain perception, basic autonomic regulation and rhythms.
monoamines involved in Bipolar disorder and major depressive disorder?
5HT, NE, DA
What role does NE play in CNS
Sleep, Arousal, Anxiety, Pain, Activation
What role does 5HT (5Hydroxytryptamine) play in CNS
** Most broadly distributed NT in the brain **
Mood regulation, Sleep, pain, agression, memory, appetite, blood pressure, respiratory and pulse rates
** 5HT in CNS decreases depression and axiety at many sites. MAY ALSO PROVOKE AGITATION, SOCIAL DYSFUNCTION AND HEADACHE
What role does DA play in CNS
Pleasure and motivation, structure cognition and emotion, regulate reward in nucleus acumbens and median forebrain bundles
What is the "finger print of depression" with regards to sleep abnormalities?
Have decreased REM latency, REM earluer and also altered periodicity. Happens in 45 - 90 minutes in normal people but earlier in those with depression.
The kindling model of mood disordrs is an endogenous process in the __________ system and might explain why these depressive episodes occur and why we can use Anti epileptic drugs for mood disorders
Limbic system
How are patients with excessive activation of hypothalamic-pituitary -adrenal axis likely to respond to antidepressants?
If challanged with dexamethasone and unable to suppress cortisol these patients are likely to have a poor response
True or False:
Patients with depression have thyroid abnormalities
True
How would you treat mild - moderate Major Depressive Disorder?
Antidepressants or pyschotherapy
How would you treat severe Depressive Disorder?
Antidepressants and pyschotherapy
Electroconvulsive therapy - works very well if pyschotic features are present
"Treatment resistant depression" is treated with
-Change the class of drugs
-ECT
-Antidepressants & Lithium or thyroid hormone
-Vagal nn stimulation
What is a mood stabilizer?
Treatment that will treat/ prevent both episodes of mania or depression and not increase the likelihood of the opposite mood state
Name the three main categories of mood stabilizers:
Lithium
Certain Anticonvulsants - Valproic acid, carbamazepide, lamotrigine
Second generation antipyschotics- Aripiprazole, Olanzapine, Quetiapine, risperidone, Ziprasidone
What is the controversy about the treatment of Bipolar disorder with antidepressants?
Thoug frequently used, they are thought to have ltd efficacy and may worsen the course of illness or switch to mania.
You are treating a patient with unipolar depression with antidepressants, what do you need to know as a physcian?
All antidepressants probably work as first
2nd line antidepressants are most frequently used (SSRI's). First line antidepressants are used for recurrent htn.
If patients recover, use the same dose that worked for an additional 6-12months, NOT LESS.
with 2 episodes of unipolar depression with antidepressants, what do you need to know as a physcian?
Continue treatment for prophylaxis for 5 years
with 3 episodes of unipolar depression with antidepressants, what do you need to know as a physcian?
Continue treatment for prophylaxis indefinately
List the 6 SSRI's found in the US
Sertraline
fluoxetine
Paroxetine
Citalopram
Escitalopram
Fluvoxamine
The only treatment of bipolar disorder shown to reduce the risk of suicide is:
Lithium
Can Lamotrigine be used to treat bipolar disorder?
Yes, can treat depressive and manic disorders in depression.
This atypical antidepressant affects both DA and Noradrenergic receptors?
Buproprion
This a pre-synaptic alpha-2 blocker antidepressant, that increases release of 5HT and NE?
Metaprazon
What is the duration of acute treatment of depression?
3wks - 6 wks, not less because it takes the medication about 2 wks to reach steady state and takes 6-8wks for marked benefit.
If one has 3 episodes of depression, what is the likelihood that they will get another?
90%, if 2 episodes 80% and if 1 episode, 50%
Risk of a child of parent with bipolar disorder having a child with bipolar?
10%
Both parents with bipolar disorder, risk of children having bipolar?
50%, advise patients on this
What NT are involved in the pathophysiology of ADHD?
NE and DA, prefrontal cortex (cognitive function and planning)
What drugs are effective in the treatment of attentional & impulsivity symptoms in ADHD patients?
Amphetamine stimulatants:
Methylphenidate - Ritalin
Dexmethylphenidate
Mized amphetamine salts

Antidepressants
Buproprion
Venlaxafine
TCA - amitryptiline, desipramine and nortriptyline


Non-amphetamine stimulants
Atomoxetine
Drugs ysed to treat hyperactivity symptoms in ADHD patients:
Alpha-2 agonists:
Clonidine
Guanfacine
Which drugs can be used to control tics worsened by stimulants in ADHD?
Alpha-2 agonists:
Clonidine
Guanfacine
Schizophrenia:
What % of population has this and what is the lifetime suicide rate of this patients?
1% of patients
10 - 15% suicide rate
Etiology associated with Schizophrenia
Genetic
Dopamine agonists - exacerbate positive symptoms
DLPFC - injury causes apathy and negative symptoms
DSM IV criteria to diagnose schizophrenia
Duration of illness = 6 months
Should have at 2 of the following positve symptoms for a continuous period of 1 month:
Delusions
Hallucinations
Thought disorder
Disorganized behavior
Negative symptoms
& this should affect their functioning
The most important complication of anorexia
Death in 8 - 18% patients - primarily by arrythmia and suicide
Patient refuses to maintain weight above 85%IBW, has missed 3 consecutive periods, has problems with her body image and intense fea of gaining weight
Anorexia Nervosa, Restrictive or purging
Patient has had recurrent binge eating and purging for @LEAST TWO DAYS A WK/3MONTHS. Also has problems with body image. What is Dx?
Bulimia Nervosa
What drug is indicated in the Rx of Bulimia nervosa?
SSRI's
Fluoxetine - treat depression that is evident in many bullimic patients
When do you admit an anorexic patient
If either:
<70%IBW
Orthostatic/ bradycardic
hypokalemic
hypoglycemic
Lab findings in anorexic patients:
All decreased except increase in cholesterol and carotene levels
ECG findings in anorexic patients:
QT prolongation
Sinus Bradycardia
Non-specific T-wave abnormalities
Lab findings in Bulimia nervosa patients:
Hypokalemic
Hypochloremic
Decr. Plasma and phosphate levels
How do you treat excessive daytime somnolence in patients with narcolepsy?
Stimulants:
- Modafinil
- Methylphenidate
How do you treat REM symptoms in patients with narcolepsy?
Antidepressants (SSRI - fluoxetine and TCA-Clomipramine)
List drugs tha are used to treat insomnia
Hypnotics - BZs and Zolpidem and Zaleplon
OTC antihistamines - Diphenhydramine
Valerian - muscle relaxant and anxiolytic
Melatonin
List Sedating antidepressants
Amitriptyline
Doxepin
Trimipramine
Nefazodone
Mirtazapine(Remeron)
Activating antidepressants:
Protriptyline
Buproprion
Most SSRI's
Venlafaxine
MAOI
What Rx would you offer one with advanced sleep phase syndrome (evening sleepiness)
PM phototherapy
What Rx would you offer one with delayed sleep phase syndrome (evening sleepiness)
AM phototherapy
What drug may be used to treat sleepwalking
Clonazepam.
(These patients sleep walk in first third of night during non-REM sleep)
Difference between sleep terror and nightmares?
Sleep terror is during NON-REM delta sleep whereas

Nightmares are during REM - cause abrupt wakening
REM sleep disorders with excessive movement may be treated with?
Clonazepam
Aqueous humor is drained to ciliary veins via?
Canal of Schlemm
Which organ makes acqueous humor?
Ciliary body
Where in the eye do you find Bruch's membrane?
Between the retina and the choroid
What type of epithelium is found in on the ciliary body and which cell layer (inner or outer is pigmented - note that both layers are part of retina)
Stratified cuboidal epithelium
Outer layer - pigmented
Which cells of ciliary body generate the aqueous humor?
Cells of the inner epithelium
What is the name given to the fibers made of fibrillin that extend from the ciliary processes of eye to lens and form the suspensory ligament of the lens?
Zonule fibers
What effect does reduced tension of zonular fibers have on the lens?
Accomodation
What is the name given to the anterior surface of the iris?
Anterior border layer - this does not have epithelium - condensation of fibroblasts and melanocytes
Part of the retina that forms the outer layer in the iris has radially oriented muscles known as
Dilator pupillae muscles
The smooth muscle cells found in the center of the iris and involved in regulating pupil size are:
Annular sphincter pupillae muscles
These are specialized glial cells form the outer and inner limiting membranes of the retina and offer support to ganglion cells:
Muller cells
Define "watershed zone" with reference to the eye:
Area between retinal and choroidal circulations