Mbchb3 Clinical

302 – CLINICAL 1

REFLEXES AND MUSCLE TONE

Nerves
Jaw jerk Trigeminal Nerve
Biceps C5/6
Supinator C5/6
Triceps C7
Finger C8
Knee L3/4
Ankle S1

UMN/LMN/Extra-pyramidal

Extrapyramidal – other than the pyramidal tract
Extrapyramidal motor system – all of the brain structures affecting bodily mvment excl motor neurons, motor cortex and the pyramidal tract (although wide def, commonly used to refer to basal ganglia (striate body), and assoc structures (substantia nigra, subthalamic nucleus and its desc connections within the midbrain)
Pyramidal Tract (corticospinal tract) – fibers originate from pyramidal cells of various sizes in 5th layer of precentral motor and pre-motor area – interruption of pyramidal tract at or below it cortical origin causes impairment of mvment on the opposite body half esp severe in leg and arm, characterized by mus weakness, spasticity and hyperflexa and a loss of discrete finger and hand mvments
Pyramidal Decussation – the intercrossing of the bundles of the pyramidal tracts at the lower border region of medulla oblongata (syn motor decussation)
Lower motor neuron – the final motor neuron that innervates skeletal muscles (distinguished from upper motor neurons of the motor cortex that contributes to the pyramidal or corticospinal tract

UMN eg stroke, spinal cord lesions, brain tumors LMN Extra-pyramidal (basal ganglia)
Wasting 0 + 0
Fasciculation 0 +/- 0
Tone ↑ (spasticity) Normal or ↓ ↑ (rigidity)
Power ↓ ↓ Normal
Tendon Reflexes ↑ ↓ or absent Normal
Plantar Response (babinski reflex – normal is flexion of the big toe) Extensor Flexor Flexor
Rapid Alternating Movements ↓ Normal ↓
Key Points
• UMN → spasticity, ↑ tendon reflex and extensor plantar response (case study – damage at C5)
• LMN → normal or ↓ tone, ↓ or absent tendon reflexes
• Extrapyramidal → rigidity and ↓ in rapid alternating mvments

Myotatic Reflex (myotasis = stretching of a mus)
Tendon Jerks
• Invol
• Non-fatiguing
• Stim strength determines degree of response
• Affected by mus activity in same segment

SENSATION

If the pt does not hav sensory sx –
• Perform a screening exam for asymptomatic abnormalities incl vibration and joint position in the fingers and toes, light touch and pin prick sensation in hands and feet

Sensory exam
• Most difficult and unreliable part of neurological exam
• Leave to the end so that sensation is tested w a spec ques in mind
• Approach to sensory exam depends on the clin prob – ex if you suspect peripheral neuropathy determine if there is a ↓ in sensation in peripheries (glove and stocking loss of sensation) or if you suspect a spinal cord lesion, look for a sensory level over the trunk or arms
• Demonstrate the stimulus over a part where you know the stimulus will be normal
• Most of the sensory exam will be done with the pts eyes closed
• Apply stimli at irreg intervals so cant be anticipated
• Don’t slant your instructions towards the abnormal eg don’t ask if it feels different
• Draw a diagram to show the sensory abnormalities

UMN (cortex or spinal cord) – weakness, ↑ tone reflex (spastic paralysis), one side of body affected
LMN (peripheral nerves) – weakness, ↓ tone reflex (flaccid paralysis), nerve root or peripheral nerve distbn
Diabetic peripheral neuropathy – only a loss in sensation

Primary Sensation Testing
1. Light touch cotton wool
2. Pain (pinprick) safety pin
3. temp hot/cold test tubes or back of tuning fork
4. vibration 128Hz tuning fork
5. joint position passive joint mvment

1. Light Touch
• Use v light touches w a fingertip (or wisp of cotton wool)
• Don’t drag your finger over the skin – this is tickling and allied to pain sensation rather than light touch
• Ask pt to say yes each time a touch is felt
• Normally – most pts detect most light touches on fingertips or toes

2 Pin Prick
• Use a large safety pin that is discarded after use
• Ensure the pt reports the sharpness of the stimulus and not a feeling of contact or pressure
• Touch the pt firmly without puncturing the skin
• Apply two or three stimuli in a localized area – a single pin prick may not register pain
• Don’t apply consecutive stimuli in same spot
• Ask pt to distinguish betw sharp (pin) and blunt (blunt end safety pin) stimuli

3. Temperature
• If pin prick sensation is tested properly – its usu not necessary to test temp

4. Joint Position
• Demonstrate which mvments are up or down while pt is looking then test w eyes closed
• Test joint position in the middle finger
• Hold the middle phalanx on each side
• With the other hand, hold either side of the distal phalanx
• Do not hold the distal phalanx betw the pulp and the nail, otherwise pres may allow the pt to identify the direction of mvment
• Move the distal phalanx up or down in random order
• Ask the pt to report the direction of each mvment
• If joint position sensation impaired – test in wrist and elbow
• In the legs – test the big toe
• Hold the proximal phalanx with one hand
• Hold the distal phalanx on each side with the other hand
• Move the distal phalanx up or down in random order
• If joint position impaired at big toe, test at ankle or knee

5. Vibration
• Use a 128 Hz tuning fork
• Demonstrate using pts sternum
• Make sure the pt reports vibration not the sound of the tuning fork or pres
• Test vibration over the pulp of the middle finger and big toe
• Pos stimuli (vibrating fork) and neg stimuli (non-vibrating fork) presented in random order
• If vibration sensation is absent over the digits, test it over the proximal bony promineneces (distal end radius, olecranon in arm, medial malleolus, tibial tuberosity, ant sup spine of ilium in leg)

6. Discriminative Sensation
• May be impaired with lesions of parietal lobe or the thalamocortical projections but isn’t routinely tested
Two Point Discrim
• Pair of dividers w blunt points
• Test over finger tips
Stereogenesis
• Can only be tested if touch, pin prick and vibration in hand are normal and if pt can move the hand
• See if pt can recog objects placed in hand while eyes closed
• Use fairly easily recog objects such as keys, safety pin
• Check normal hand first
Graphaesthesia (number writing)
• See if pt can recog single digit numbers traced on palm of hand
Bilateral simultaneous stim (sensory inattention)
• Touch the pt’s right hand or L hand separately or simultaneously in random order
• Ask pt to report which side is being touched

7. Deep Pain
• Do not test routinely
Deep pain may be intact even when pin prick sensation is abnormal

Dermatomes
• C3 – neck
• C6 – thumb and forearm thumb side
• C7 – middle finger
• T4 – nipple
• T10 – umbilicus
• L1 – inguinal
• S1 – lateral foot

NERVOUS SYSTEM

Two impt questions to answer –
1. Where is the lesion?
2. what is the cause of the lesion?

Parts of the Nervous system examination –
• mental status
• language
• cranial nerves
• limbs/trunk (motor sys, reflexes and sensation)

MOTOR SYSTEM EXAMINATION (SUMMARY)
1. Intro
2. General Observations
3. Tone
4. Power
5. Coordination
6. Reflexes
7. Posture and gait
8. Conclusion

1. Intro
• Introduce yourself
• Position lying comfortably with pillow
• Expose upper and lower limbs
2. General observations
• Observe the muscles for any wasting, fasciculations, scars and abnormal mvments
• Fasciculations – Involuntary contractions, or twitchings, of groups (fasciculi) of muscle fibers, a coarser form of muscular contraction than fibrillation
• Upper arm drift – shoulder level with palms up and eyes closed for 10-15 secs – look for drift of one arm (or pronation) – unilateral drift often indicates that there is an abnormality of the nervous sys, but is not helpful in localizing the lesion
3. Tone
• Assess at elbow, wrist, knee and ankle – flexion and extension but also pronation/supination at wrist
• Normal or increased? (spastic, cogwheel, lead pipe rigididy) – is there clonus?
• Clonus - A form of movement marked by contractions and relaxations of a muscle, occurring in rapid succession seen with, among other conditions, spasticity and some seizure disorders
• Spasticity - A state of increased muscular tone with exaggeration of the tendon reflexes – to test: eg arm – pull arm toward you passively and rapidly, if it contracts against you, then lets go, this is spastic
4. Power
• Distal to proximal
o Finger flexion/extension/abduction
o Wrist flexion/extension
o Elbow flexion/extension
o Shoulder abduction/adduction
o Great toe dorsiflexion/plantar flexion
o Ankle dorsiflexion/plantar flexion
o Knee flexion/extension
o Hip flexion/extension
• Move from side to side at each group, comparing L and R
• Other muscle groups may be tested if clinically indicated
• Remember to grade degree of any weakness
5. Co-ordination
• Finger-nose test – look for tremor as in the last few cm as the finger approaches the target – don’t move the target
o An intention tremor may be masked by holding the target too close to the pt, moving the target or asking the pt to perform the test too quickly
• Rapid alternating movements (upper and lower limbs) – hand tap, foot tap
• Heel-knee test
6. Reflexes
• Finger, supinator, biceps, triceps jerks
• Knee and ankle jerks
• Remember to grade the strength of the reflexes
• Remember to reinforce (augment) the reflexes if unable to see them
• Plantar response (with a key)
7. Posture and Gait
• Observe pt walking normally w arms at side
• Note pressure, stride length, broadness of base, arm swing, steadiness/smoothness
• Walk heel to heel (like on a tightrope)
• Romberg’s test – stand w feet together w eyes closed
8. Conclusion
• Offer to help pt with dress (nb autonomy/dignity)
• Thank pt

General Points – Examining the Motor System
Tone
• Tone is resistance to passive mvment of a limb
• Pt must be relaxed
• ↑ tone may be due to rigidity (in diseases affecting the basal ganglia eg Parkinson’s)
• ↑ tone may be due to spasticity (in diseases affecting UMNs)
• ↑ tone may be difficult to distinguish from voluntary mus contractions due to poor relaxation
Rigidity
• detected w slow passive mvment of a joint
• there is uniform resistance throughout stretching the mus and it may be assoc w cog-wheeling (jerky interruption of mvment)
• it affects flexors and extensors in a limb about equally
Spasticity
• detected with rapid passive mvment
• tone is maximal at the start and then ↓ suddenly as the mus is lengthened (clasp knife phenomenon)
• it is marked most in flexors in the arm and extensors in the legs
• sudden stretching of a spastic mus produces reflex contraction
• if stretch is maintained, further reflex contration w repetitive beating (clonus) occurs
• clonus is usu most marked in the ankle plantar flexors
Power
• ask the pt to complete the mvment and then maintain mus contraction while you try to overcome it
• provide stability by holding the pts limb proximal to the joint being tested
• note the distbn of weakness – this is more impt than the severity of weakness
• Scale – (MRC scale) -
o 0 – non contraction
o 1 – a flicker or trace of contraction
o 2 – active mvment with gravity eliminated
o 3 – active mvment against gravity but not against resistance
o 4 – active mvment against gravity and against resistance, but reduced power
o 5 – normal power

Motor Examination of the Arms
• examine the arms w the pt sitting on the side of the bed or in a chair
• observe the arms at rest and then held outstretched
• asses tone at the wrist and elbow (incl supination) – spasticity occurs on supination (soup bowl)
• use the screening examination of power
• test coordination (rapid alternating mvments and finger nose finger test)

Motor Examination of the Legs
• observe the legs while the pt is standing, walking and lying
• assess tone at the knees and check for clonus of the ankles
• use the screening evaluation for power
• test coordination (rapid alternating mvments and heel-knee-shin test)
Tone
• check for spasticity in the leg extensors by placing both hands under the pts knee
• when the pt is relaxed, quickly lift the knee up in the air – if tone is normal, the pts heel drags up the bed – in a spastic leg, the foot flicks up in the air and then drops to the bed (clasp knife phenomenon)
Clonus
• flex the hip and knee to about 45 degrees and externally rotate the hip
• rapidly dorsiflex the foot and maintain foot in this position
• if there is spasticity in the calf muscles, this may provoke clonus
• 2 or 3 beats of clonus may be present in normal people, but it should be similar on each side
Coordination
• rapid altenating mvments – if sitting, ask pt to rapidly tap the ground with the sole of the foot, if lying, ask the pt to lift the leg off the bed and shake it at the ankle
• point to point (heel knee shin) – ask the pt to elevate one foot, place the heel on the other knee, and slowly run the heel down and up the shin

Tendon Reflexes
• test biceps or brachioradialis (supinator), triceps, knee and ankle reflexes and also test plantar responses
Biceps Reflex
• C5/6
• Place index finger on biceps tendon
Brachioradialis (supinator) reflex
• same nerve root as biceps – C5/6 → dont check both
• easier to test than biceps reflex
• position the pts arm as for the biceps reflex w forearms midway betw prone and supine
• place index finger on distal end of the radius and strike finger w reflex hammer
Triceps
• C7
• Place pts forarm across the abdomen w elbow flex to 90 degr
• Strike triceps tendon directly
• Alternatively – test the reflex while supprting the pts arm at the elbow w the shoulder abducted to 90 degr and the forearm haning
Finger Reflex
• C8
• not tested routinely but can be helpful in pts you suspect of having a C8 nerve root lesion
• hold pts fingers w your fingers and extend the pts fingers slightly
• tap your fingers gently
• the finger reflexes are absent in many normal people, but unilateral absence of a finger reflex is abnormal
Knee Reflex
• L3/4
• Flex the knee to 90 degr
• Support the thighs w the heels resting on the bed
• Strike the patellar tendon
• Alternatively have the pt sit w the leg legs hanging free over the edge of the bed
Ankle Reflex
• S1
• Can be tested in 3 ways
o W pt supine – place your hand on the sole of the pts foot and passively dorsiflex the foot to 90 degr
 Strike your hand with the hammer
 This is the easiest method of eliciting an ankle reflex but is also the least sensitive
 If this does not elicit a reflex, proceed w one of the other methods
o with the pt supine, flex and externally rotate the pts hip and flex the knee
 gently dorsiflex the pts foot to 90 degr and strike the Achilles tendon directly w the hammer
o have the pt kneel on a chair w feet hanging over the edge
 strike the Achilles tendon directly w the hammer
 this is the most sensitive method of eliciting an ankle reflex
Reinforcement of reflex
• can be reinforced if uncertain whether a reflex is present or not
• when testing the arm reflexes, ask the pt to clench the jaw
• for the leg reflexes, ask the pt to interlock the fingers of both hands and pull just before you strike the tendon
• some normal people have no tendon reflexes, tendon reflexes in the legs are more active than in the arms, esp for young peop
• anxious people may have v brisk tendon reflexes
Grading of tendon reflexes
• 0 absent
• +/- just present
• + normal
• ++ brisk normal
• +++ v brisk
Plantar Responses
• try to put pt at ease
• firmly draw a blunt object (eg a key) up the lateral border of the sole of the foot and then across the ball of the foot
• you may need to repeat this test several times while applying varying degrees of pres
• the normal response – flexion of the big toe (flexor plantar response)
• in an UMN lesion – big toe extends up and the other toes may fan out (extensor plantar response or babinski reflex)
• record as flexor, extensor or no response

SENSORY SYSTEM EXAMINATION (SUMMARY)
1. Intro
2. General Points
3. Light touch
4. Pin prick
5. Joint position
6. Vibration
7. Discriminative sensation
8. Conclusion

1. Intro
• Introduce yourself
• Position, lying comfortably w pillow
• Expose upper and lower limbs as appropriate
2. General points
• Demonstrate the stimulus over part where you know it will be normal
• Test sensation w pts eyes closed
• Test systematically (by dermatomes)
• Test L and R sides as you go
• Apply stimuli at irreg intervals so pt cant anticipate
• Once an abnormal area identified map it further by moving from area of abnormal to normal sensation
3. Light touch
• Use v light touch w wisp of cotton wool (don’t drag the cotton wool over the skin)
4. Pin prick
• Use a new safety pin and discard after use
• Use sharp side of pin but every so often use blunt side
• Ask if it feels sharp or blunt
• Remember that you are testing pain sensation (not blunt)
5. Joint Position
• Test in great toes first (if normal don’t need to test more proximally or in the upper limbs)
• Hold the middle phalanx at the sides to steady joint and hold distal phalanx at the sides w the other hand
• Gently move joint up and down
• Ask pt “is this moving up or down?”
6. Vibration
• Use a 128Hz tuning fork
• Demonstrate normal on upper sternum
• Place tuning fork over bony prominence (start at dorsum of DIP joint of great toe – if normal don’t need to test more proximal joints or in upper limbs)
• If abnormal, test more proximally and in the upper limbs
• Remember you are testing vibration, not the ability to feel the tuning fork
7. Discriminative Sensation
• Not tested routinely but be aware of it
8. Conclusion
• Offer to help pt w dressing (nb autonomy, dignity)
• Thank pt

Mental Status
• if the pt is alert, gives clear hx, answer questions and obeys instructions briskly and accurately, mental status is probably normal
• if you suspect impaired mental status, perform a more detailed assessment incl orientation, memory, abstact thinking and calculation

Language
• if pt does not speak fluently, has difficulty following instructions or understanding questions, or appears confused, a more detailed assessment of language is reqd
• a full assessment includes analysis of spoken and written responses to both spoken and written questions

HEMIPARESIS

Hemiparesis – unilateral weakness (face, arms and legs)
Hemiplegia – unilateral paralysis
Paralysis – loss of power of vol mvment in a mus through injury or dis to or of nerve supply, loss of sensation

Pyramidal Lesions (UMN lesions)
• Weakness
o Upper limbs – flexors weak BUT stronger than extensors
o Lower limbs – extensors weak BUT stronger than flexors
• ↑ tone – Spasticity (spastic catch aka clasp-knife)
• ↑ reflexes (on side of weakness)
• extensor plantar response (babinski – big toe goes up not down)
Other signs
• no wasting or fasciculations
• impaired alternating rapid mvments

LMN Lesions
• weakness (like UMN lesions but pattern different)
o Pattern of weakness depends on which nerve root or peripheral nerve is damaged
o Eg C5 nerve root lesion → shoulder abduction weakness
• ↓ tone (flaccid paralysis)
• ↓ reflexes
• ↓ plantar response

Ex – Spinal compression at L1
• above L1 – UMN pattern of weakness
• below L1 – LMN pattern of weakness
Ex – Spinal compression at T10
• ↑ tone in legs
• ↑ reflexes in legs
• Pos babinsi
• Loss of sensation distal to umbilicus

Acute Subdural Hematoma – R Side

Stroke

• A group of disorders involving hemorrhage or occlusion of brain blood vessels
• Worldwide – 3rd leading COD
• More common in older people
Main types of Stroke
• Ischaemic
o 50% contributed to by atherosclerosis of extra-cranial arteries
o 20% by emboli from heart
o 25% occlusion of deep arteries
• Hemorrhagic
• Stroke is mostly focal (loss of blood supply to a partic area of the brain) but can be global (eg caused by cardiac arrest)
Risk Factors
• Diabetes
• HT
• Atherosclerosis
• Genetic polymorphisms
Focal Ischaemia - Core/Penumbra
• Nerve cells in brain region w greatest loss blood flow in focal ischaemia (core or infarct zone) die rapidly by necrotic mechanisms (cell death)
• Around infarct is region called penumbra where nerve cells die slower (24-72 hrs – delayed cell death) via apoptic process (cell suicide)
• Necrotic death probably occurs too rapidly to be amenable to therapeutic intervention – hence most therapy has focused on rescuing nerve cells in the penumbra
Causes of Necrosis
• Cell Lysis
Causes of Delayed Cell Death - Hypotheses
• massive glutamate release (saturation of transporters)
• influx of intra-cellular Ca2+
• free radical prodn
• activation of brain macrophages (microglia) releasing NO, superoxide, cytokines
• activation of intrinsic apoptotic mechanisms

Excitotoxicity Theory
• one theory to explain how neurons die during stroke
• excitotoxicity theory = excessive activation of glutatmate systems in the brain → nerve cell death
• saturation of glutamate transporters may be involved here
• the NT glutamate functions normally in learning and mem, mvment and sensation
Glutamate Receptors
• Ionotropic (ion channels) – NMDA, AMPA/Kainate
• Metabotropic – G protein linked
NMDA Receptors – see diagram
• N-methyl-d-aspartate
• Glutamate binding site
• Glycine binding site (co-agonist)
• Ligand and voltage-gated channel
• Depol thus requires both glutamate and glycine to open channel → Ca2+ influx → neuon depol
• Mg – occupies and blocks channel
• Depolarization → Mg efflux (hence voltage dependent) – now ligand is able to bind (ligand dependent)?
• PCP – penycyclindine aka angeldust – binds inside channel → block of ion flow (non-competitive antagonist)
• NMDA antagonists are generally neuroprotective but complex
AMPA Receptors
• Ligand-gated ion channel
• Glutamate binding → Na+ influx → neuronal depol
• Receptors composed of multiple sub-units: GluR1-4
• Receptors w GluR2 sub-unit pass Na but no Ca
• Receptors without GluR2 but with GluR3 can carry Ca ions
• Ischaemic brain injury causes down-reg of GluR2 subunit – might act to promote brain damage by ↑ Ca Fluxes
Kainate Receptors
• Composed of subunits: GluR5-7
• Ligand gated ion channel
• When glutamate binds → Na Influx → Neuronal depol
Metabotropic (G protein linked receptors)
• Group 1 (mGluR1&5)
o Glutamate binding → phosphoipase C → depol neurons
o Group 1 antagonists are neuroprotective in mdoel systems
• Group 2 (mGlu2&3)
o Gi linked and inhibit adenylate cyclase and cause inhibition of NT release
o Agonists at these receptors are neurorprotective in model systems

Model
• Stroke → Excitatory AAs, ↑ glutamate → pathological activation of AMPA, NMDA and mGluR1/5 receptors → BOTH:
o ↑ Ca2+ (NMDA) → delayed n cell death (hours/days) via apoptosis
o ↑ Na/↑Cl/↑H20 (AMPA) → rapid nerve cell death (mins) via cell lysis/necrosis
• how mGlu1/5 contribute to n cell death is not clear but Ca released from intracellular stores could be involved
Calcium and Cell Death
• ↑ Ca → activation of Ca sensitive enzymes → programmed cell death/apoptosis/necrosis
• eg – biochem pways intrinsic to neuron are activated → cell death by suicide eg cleaved caspase 3
• these intracellular n cell death pways are beginning to be dissected out and novel targets to treat neurodegeneration are being described and drugs developed
• n cell survival pways are also being discovered
• a number of studies suggest that ischaemic neuronal cell death requires new gene expression which activates caspase enzymes that cleave substrates leading to cell death – caspases 1,2,3,8,9 and 12 are activated themselves by cleavage and then target substrates leading to neuronal aoptosis
• caspase 3 is partic impt in neuronal apoptosis
Neuronal Apoptosis
• Stroke → activation of death inducing transcription factors → activation of apoptotic machinery (eg caspases) → neuronal cell death

Treatments
• TPA – tissue plasminogen activator – for thrmbolysis but must be given within 3 h of stroke (only 3-5% eligible and only 13% of these benefit)
• Glutamate acting drugs have not yielded good results in clinical trials to reduce brain injury – reasons for this lack of efficacy is unclear but may be due to –
o That activation of NMDA receptors can under some conditions be neuroprotective – ie synaptic NMDA Receptor activation via glutamate elicits neuronal survival while activation of extra-synaptic NMDA receptors elicits neuronal cell death
o Ischaemic tol developws – where a brief period of ischaemia protects the brain from subseq normally injurious ischemic insult, depends upon activation of NMDA receptors
o Thus the role of NMDA receptors and glutamate in brain injury is complex
• Hypothermia – may work, small effect possible
• Free radical scavengers – disappointing results
• Anti-inflam meds – to block microglial active disappointing
• Blockers of caspase – potential
• Stroke stem cells in brain may be activated to generate new neurons to replaced cells that died – microglia activeated in the region of stroke may act to guide migration of these new cells into the region of cell loss
• Currently no effective n rescue therapy for stroke

SCHIZOPHRENIA

Lecture Slides

Objectives
• introduce psychiatric classification sys
• define terms psychotic and neurotic
• describe clinical feats of schizophrenia and major mood d/o
• outline the diathesis-stress model of mental d/o

Key Concepts
• mental health – state of emoal and soc wellbeing
• mental health probs – wide range of emoal and behal abnormalities that affect peop throughout their lives
• mental d/o – a clinically recog set of sx and behs which usu need tx to be alleviated – serious departure from normal functioning

Psychotic Disorders
• Experiences are qualitatively diff than normal experience eg hallucinations
• Involve the whole personality
• Usu assoc w loss of reality testing – there is a loss of insight
• Beh may be conspicuously disordered
• Eg – schizophrenia, bipolar mood d/o

Neurotic Disorders
• Experiences are diff in quantity – eg excessive anxiety
• Do not involve the whole personality
• Insight usu retained
• Beh may appear to be normal except in certain circumstances
• Eg – agoraphobia, obsessive-compulsive d/o

SCHIZOPHRENIA

Dx of Schizophrenia – DSM4
• Pos sx – delusions, hallucinations, disorganized speech and/or beh
• Neg sx – amotivation, restricted affect, poverty of speech
• Soc/Occup dysfunction
• At least 6 months duration
• Not due to gen med condition, drug use or any other mental d/o
Notes
• Abnormality is reflected in discrete sx – sx fall into discrete clusters called syndromes
• DSM4 – multi-axial sys of dx
o Axis 1 – the dx
o Axis 2 – personality d/os
o Axis 3 – physical complications
o Axis 4 – precipitating factors
o Axis 5 – global assessment of function
Schizophrenia - Syndrome based on a process of psychological disintegration manifesting itself ultimately as a fragmentation of the personality
Epidemiology
• Lifetime risk – 1%
• Annual incidence – 1/10000
• M=F
• Females may have better outcome
• Onset in males earlier (15-25 yrs cf 25-35 yrs)
Clinical Feats
• Prodromal phase – social withdrawal, loss of interest, irritability, poor self care, vague unease or anxiety
• Acute phase – delusions, hallucinations, disorganized speech
• Residual phase – amotivation, social withdrawal, restricted affect, poverty of speech
• Subtypes – paranoid, disorganized, catatonic, undifferentiated, residual
• Course – variable
Etiology
• Unknown
• Both genetic and etal factors appear impt
• Interaction betw vulnerability and stress
Genetic Factors
• Family, twin and adoption studies
• First degree relatives – risk is 10-15%
• Monozygotic twins – 50% risk cf dizygotic twins – 10-15%
• Adoption studies – show risk depends on biological parentage
• Eye movement abnormalities and/or changes in event related potentials may be biological markers of genetic predisposition
Environmental Factors - Biological
• CT/MRI/PET/SPECT/neuropsychological/neuropathological studies
• Suggest abnormalities in brain structure and func in some subjects w schizophrenia (mainly frontal and temporal lobes)
• Obstetric complications and viral infections during intrauterine devt may contribute
• Drug use – eg amphetamines, PCP, cannabis may precipitate relapses
Environmental Factors – Psychosocial
• Stress may act as precipitant for relapse
• Stress may be due to events (eg loss) or be interpersonal
• Major stresses arise from social factors – poor housing, poverty, isolation
• Too little stimulation may ↑ negative sx
Mediating Factors
• Overactivity of dopamine neurons in meso-limbic sys (dopamine hypothesis)
• Alteration in ability to focus attn may lead to difficulties in info processing
Tx
• Antipsychotic drugs – chlorpromazine, haloperidol – block dopamine and are good for neg sx but have side effects
• New drugs – clozapine, risperidone – reported to have greater effect on neg sx
• Education
• ↓ interpersonal stress – problem solving, communication skills
• ↓ social stress – help w accom, work etc

MOOD DISORDERS

• Mood – internal feeling or emotion which often influences beh and perception of the world
• Affect – external expression of an emoal state
Mood Disorders
• Characterized by episodic alterations in mood separated by periods of euthymia (moderation of mood, ie mental peace)
• The episode or changed mood may be primarily depressive, primarily manic or mixed
• Mood d/os are classified as unipolar (major depr) or bipolar (manic-depressive)
• Bipolar 1 – manic and depressive episodes
• Bipolar 11 – hypomanic (mild mania) and depressive episodes
Major Depressive Episode
• 5 or more of following sx over two weeks for most of day and nearly every day
o depressed mood, anhedonia (absence of pleasure in otherwise pleasurable acts)
o weight change, sleep disturbance
o agitation or restlessness, fatigue or loss of energy
o loss of concentration and indecisiveness
o feelings of worthlessness and guilt
o recurrent thoughts of death or suicide
o not 2ndry to drug use or med d/o
Manic Episode – DSM4
• elevated expansive or irritable mood for more than 1 k plus three or more of –
o grandiosity, decreased sleep, talkative, racing thoughts, flight of ideas, distractable
o ↑ in goal directed activity
o excessive involvement in pleasurable experiences w high potential for adverse conseqs
o not due to drugs or med condition
o hypomania similar but less severe
Etiology
o both genetic and etal factors impt
o interaction betw vulnerability and stress – diathesis-stress model – ie you inherit a predisposing vulnerability but the disease process depends on etal circumstances
o diathesis = the constitutional or inborn state disposing to a disease, grp of diseases or metab/structural anomaly
Mediating Factors
o Neurodevelopmental Hypothesis - Genetic predisposition +/- etal factors leads to incorrect synaptic connections, poor migration of neurons
o Neurodegenerative Hypothesis - Glutamate excitotoxicity secondary to pos sx leads to degen of neurons
o Overactivity of dopamine neurons in mesolimbic sys of brain (dopamine hypothesis)

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