Tutorial Psychia 56

7/30/2019 Tutorial Psychia 56

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Psychiatry tutorial

Surat Tanprawate, MD, FRCP(T)

Division of Neurology, Chiang Mai University

11.05.2013


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Neurology and neuropsychiatry

Neurological disorders that present with cognitive, and

behavioral disfunction: frontal lobe syndrome, temporal lobe

epilepsy, etc.

The disorder that combine neurology and psychiatry

manifestation: Alzhermers disease, Huntingtons disease, etc.

Psychiatric consequence of neurological disease: post-stroke

depression

Functional symptoms in neurology


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Outline

Clinical symptoms a/o syndromes

mood/affect lability, personality alterations, psychosis

(hallucination/illusion), obsessive-compulsive disorder, dissociative

disorder, alter sexual behavior/paraphilic disorder

disorder of consciousness, delirium and dementia, amnestic disorders,

aphasia, alexia, agraphia, apraxia, disorder of visual processing, frontal

lobe syndrome

Common diseases

dementia, movement disorder, epilepsy, stroke, headache


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Clinical

symptoms/syndro

mes

Mood and affect lability


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Lability of mood and affect

Lability of mood

rapid shift of one mood state to another

orbitofrontal cortex dysfunction, basal ganglia disorder(HD)

Lability of affect

sudden changes in emotional expression

eg. pseudobalbar palsy, epileptic seizure


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Pseudobu lbar palsy

Bulbar palsy refers to bilateral

impairment of function of the cranial V,VII, IX, X and XI, which occurs due tolower motor neuron lesion either atnuclear or fascicular level in the medullaroblongata or from bilateral lesions of thelower cranial nerves outside the brainstem

Balbar: LatinBulb: A globular or fusiformanatomical structure or

enlargement.Bulbus: swollen root

The Brainstem


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Pseudobu lbar palsy

Pseudobulbar palsy resultsfrom an upper motor neuronlesion to the corticobulbarpathway in the pyramidal tract.

Symptoms:

-difficulty chewing, swallowing-slurred speech (often initialpresentation)-inappropriate emotionaloutbursts.

Pathological laughing and crying


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Pathological Laughter


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Pathological crying

QuickTime and adecompressor

are needed t o see this picture.


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Distinguishing types of crying:

Pathological crying linked to infarct in basis of pontis and

corticobulbar pathways and occurs in response to mood

incongruent cues.

Emotionalism is crying that is congruent with mood

(sadness) but patient is unable to control crying as they

would have before stroke.

Catastrophic reaction is crying or withdrawal reaction

triggered by a task made difficult or impossible by a

neurologic deficit (e.g. moving a hemiplegic arm)

associated with post-stroke depression


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Epileptic seizure

A gelastic seizure

sudden burst of energy, usually in the form of laughing orcrying

Cause: hypothalamic hamartomas, temporal and frontal lobe

lesion

Frontal lobe and temporal lobe epilepsy


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Personality alteration in neurological disorder

Apathy

FTD, AD, medial frontal lesion, basal ganglia, vascular dementia

Disinhibition

Orbitofrontal lesion, caudate disorder(HD)

Irritability

Orbitofrontal lesion, caudate disorder(HD)

Explosive

Posttraumatic encephalopathy, HD

Plascidity

Kluver-Busy syndrome with bilateral temporal lobe dysfunction


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Clinical

symptoms/syndro

mes

Hallucination and illusion


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Hallucination and illusion

Hallucination=sensory experiences occurring without

stimulation of the relevant sensory organ

Illusion=misperceptions of external events

Hallucinations may involve all sensory modality

Hallucinations: simple (unformed) vs formed


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Visual pathway

Eye

Opticnerves

Geniculocalcarine projections

Occipitalcortex

Temporallobe


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Complex visual hallucination

3 basic underlying mechanism

irritative processes in the association cortex generating

discharges falsely interpreted as due to sensory input

release phenomena due to defective visual input causing faulty

cortical stimulation

faulty visual processing in which inputs are normal but lesionsresult in an inappropriate pattern of cortical excitation

Manford M, and Andermann F. Brain 1998;121, 1819-1840


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Common causes of complex visual

hallucination

Migraine aura

Epilepsy

Charles- Bonnet syndrome

Peduncular hallucinosis

Treated idiopathic Parkinsons

diseaseLewy body

dementiaNarcolepsy-cataplexy

syndromeSchizophreniaDelirium


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a uc na on o e cere racortex

Destructive lesion: release hallucination

Neuronal hyperexcitability: migraine and

epileptic seizure


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A 37 Y.O. man with

abnormal visual

symptoms for 2 weeks QuickTime and adecompressor

are needed to s ee this picture.

Release hallucination from

temporo-occipital lobe

infarct


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Michael B. R. et al. Brain1996: 119, 355-361

n=163

99% 31%

6%

18%

Typical aura:

-Visual

-Sensory

-Speech

Migraine Aura


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Typical aura

Typical aura consisting ofvisual and/or

sensory and/or speech symptoms.Gradual

development, duration no longer than onehour, a mix of positive and negative features

and complete reversibility characterize the

aura which is associated with a headache that

does not fulfill criteria for Migraine withoutaura.


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Typical visual aura is simple

Visual aura


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Blindness, visual hallucination and

Charles Bonnet syndrome(CBS)

Charles Bonnet, Swissphilosopher whodescribed CBS in 1760

The disease is named after the Swissphilosopher, who described the conditionin 1769.

He first documented it in his 89-year-oldgrandfather who was nearly blind fromcataract in both eyes but perceived men,women, birds, carriages, buildings,tapestries, physically-impossiblecircumstances and scaffolding patterns.


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Charles Bonnet syndrome(CBS)

prevalence: 1%-10%

mentally healthy people with often significant visual loss from eye

or optic pathway

visual hallucination: vivid, complex, recurrent

sufferers understand that the hallucinations are not real

Rx: It usually disappears within a year

SSRI may be helpful


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Peduncular hallucinosis

Hallucination of the midbrain

Described a 72-year-old womans visualhallucination of colorfully dressed people andchildren which occurred at dusk. Thehallucinations occurred during normalconscious state and the patients neurologicalsigns were associated with thosecharacteristic of an infarct to the midbrain and

pons. Von Bogaert, Lhermittes colleague,named these type of hallucinationspeduncular in reference to the cerebralpeduncle as well as to the midbrain and itssurroundings.

LhermitteFrench neurologist


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Visual halluc ination w ith

Park insonism

Parkinsonism is the syndrome including

bradykinesia, plus one of following

resting tremor, cogwheel rigidity, and postural

instability

Parkinsonism can be broadly divided as typical

parkinsonism(Parkinsons disease) and atypicalparkinsonism


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Visual halluc inat ion w ith

Park insonism

Parkinsons disease with visual hallucination

Usually occur in PD who taking levodopa

Atypical parkinsonism

Dementia with Lewy Bodies(DLB)

Parkinsonism, dementia, vivid visual hallucination,

and fluctuation of consciousness

C i f DLB ith AD d PD


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Comparison of DLB with AD and PD

DOUG NEEF.Am Fam Physician 2006;73:1223-9,


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Visual hal lucinat ion in DLB

Psychotic symptoms: 80 % of the patients

Visual hallucination: purely visual, vivid, colorful, 3-dimensional

hallucinations of humans or animals

DLB patient can experience severe reactions to antipsychotic

medications

Treatment

avoid antipsychotic, treat with cholinesterase inhibitors


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Visual halluc inat ion in

schizophrenia

Schizophrenia Organic cause

Animals and figures may beprominent

Usually in colour

with auditory hallucination

occur throughout working hours

less paranoid and thoughtdisorder more insight associated with abnormal

physical signs/symptoms

more often nocturnal, and areassociated with drowsiness


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Complex visual hallucination in focal

epilepsy

usually brief, sterotyped and fragmentary

associated with other seizure manifestation

Strong evidence: EEG recording


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Disorder of consciousness

Clinical

symptoms/syndrom

es


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Arousal and awareness, the two components of consciousness in

coma, vegetative state, minimally conscious state, and locked-in

syndrome.


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Behavioral state confused with coma


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Behavioral state Definition Lesion Comment

Locked-in

syndrome

Alert and aware, quadriplegic

with lower CN palsy

Bilateral anterior pontine Similar state:severe

polyneuropathyMG, NM blocking agent

Persistent

vegetative state

Absent cognitive function but

retain vegetative component

Extensive cortical grey

and subcortical white

matter with relative

preservation of brain stem

Synonyms include apallic

syndrome, coma vigil,

cerebral cortical death

Abulia Severe apathy, patient neitherspeak nor moves

spontaneously

Bilateral frontal medial Severe case resemble

akinetic mutism, but

patient is alert and aware

Catatonia Mute, and mark decreasemotor activity

Usually psychiatric May be mimicked by

frontal lobe dysfunction

and drug

Pseudocoma Feigned coma

Behavioral state confused with coma


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Locked in

syndrome


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Apathy Abul iaAkinet ic

mut ism

Diso rders of Dim inished Mot ivat ion

DDx

Those in which diminished activity is actually due to another impairment

Stupor or coma, delirium, aprosodia, catatonia, akinesia

Those in which diminished activity is associated with diminished

motivation but both are due to some other disorder

depression, demoralization, dementia


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Motivat ional ci rcu i t ry.

Robert S. Marin,. J Head Trauma Rehabil.2005:4(20)377-388

Conditions associated with apathy, abulia, and akinetic mutism


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Conditions associated with apathy, abulia, and akinetic mutism

Robert S. Marin,. J Head Trauma Rehabil.2005: 4(20)377-

388


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Frontal Lobe Syndrome

Clinical

symptoms/syndrom

es


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Phineas P. Gage

QuickTime and a

YUV420 codec decompressorare needed to see t his picture.

Phineas P. Gage (18231860)was an American railroad constructionforeman now remembered for survivingan accident in which a large iron rodwas driven completely through hishead, destroying much of his brain's leftfrontal.


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Prefron tal co rtex

Prefrontal cortex mediates complex human behavior, and three major

behavioral syndromes associated with prefrontal dysfunction have been

identified

Dorsolateral prefrontal area

Orbitofrontal area

Anterior cingulate area


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Generalorganizat ionof

the fronta l-subcort ica l ci rcu i ts

Cummings JL.Arch Neurol. 1993;50:873-880


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3 dist inc t cor t ical subco r t ical ci rcu i t

Organization of the three frontal-subcortical circuits in which lesions produce alterations ofcognition and emotion. VA indicates ventral anterior; MD, medial dorsal.

Cummings JL.Arch Neurol. 1993;50:873-880


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Orbitofrontal cortex

Anterior cingulate gyrus

Symptoms of f rontal lobe dys funct ion

aphathy

disinhibition

anosmia


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Symptoms of f rontal lobe dys funct ion

Executive function planning, initiating,sequencing(maintaining, alternating, stopping),

and monitoring behaviorExecutive dysfunction poor strategiesincluding impaired planning when copying

constructions and when organizing material to be

remembered

impaired set shifting in response to changingtask contingencies

abnormalities of motor programming compromised attention


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Aphasia

Clinical

symptoms/syndrom

es


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Aphasia

Aphasia refers to an impairment in linguistic

communication produced by brain dysfunction

It must be distinguished from other disorders ofverbal output such as dysarthria, mutism, and the

abnormal language production of patients with

thought disorder


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Language test

Speech fluency

Comprehension

Repetition

Naming

Writing


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A: Wernicke's areaB: concept center

M: Broca's area

a--> A

-auditory input to Wernicke's area

M --> m

-motor output from Broca's area

A --> M

-tract connecting Wernicke's and Broca's areas

A --> B

-pathway essential for understanding spoken

input

B --> M

-pathway essential for meaningful verbal

output.

Lichtheim's diagram of the language system

Conduction aphasia

Transcortical

sensory aphasia

transcortical motor

aphasia

Pure

word

deafness

Articulatory

disorder

(aphemia)

Sensory

aphasia

Motor

aphasia


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Aphasia chart


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Broca had the opportunity to examine the brain of a

language-impaired patient, M. Leborgne, when it

came to autopsy.

The patient had been capable of very little speech

although his comprehension appeared well preserved

Pierre Paul Bro ca (1824 1880)

French physician

Brocas aphasia


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He saw a patient whose comprehension was severely

impaired; when the patient came to autopsy, the lesion was

discovered in the posterior, superior left temporal lobe

Wernicke hypothesized that this area was the locus of

storage of "auditory word images," which were necessary for

the production as well as the comprehension of speech.

Carl Wernick e(1848-1905)German physician, psychiatrist,

neuropathologist

Wernickes aphasia


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Common neurological diseases

Alzheimers disease and dementia syndromes

Parkinsons disease and other Parkinsonism

Headache disorders


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Common diseases

Parkinsons disease and other

Parkinsonism


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James Parkinson,London

(1755 1824)

An Essay on the ShakingPalsy(1817)

Shaking Palsy(Paralysis agitans)

He identified 6 cases, 3 of whom he personallyexamined; 3 he observed on the streets ofLondon

J Neuropsychiatry Clin Neurosci2002;14:22336

P l i it


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Rigidity

Stooped posture

Hips and knees

slightly flex

Tremor

Short shuffling

steps

Reduce arm swing

Paralysis agitan

(shaking palsy)


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Parkinsonism

clinical syndrome of bradykinesia, restingtremor, cogwheel rigidity, and postural instability

Parkinsons disease

clinical syndrome of asymmetrical parkinsonism,usually with rest tremor, in association with the

specific pathological findings of depigmentation

of the SN as a result of loss of melanin-ladendopaminergic neurons containing eosinophilic

cytoplasmic inclusions(Lewy bodies)


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Something look alike

Gait disorder

Tremor: severe essential tremor,cerebellar tremor

Depression

Psychomotor retardation Frontal lobe syndrome

Group of Park inson ism P ki di


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Group of Park inson ism Parkinsons disease Secondary park inson ism hydrocephalus, vascular

parkinsonism, encephalitis, druginduced parkinsonism

Park inson plus synd rome Progressive supranuclear

palsy(PSP), corticobasaldegeneration(CBD), multiple systematrophy(MSA), Dementia of LewyBodies(DLB)

Hered itar arkinson ism

TYPICAL ORCLASSIC

ATYPICAL


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Parkinsons

disease


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Gibb et al, 1988, Table from Litvan et al, 2003


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PD- d iagnost ic c r i ter ia

Gibb et al, 1988, Table from Litvan et al, 2003

Diagnosticaccuracy to 82%


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Non-motor symptoms

Loss of sense of smell, constipation

REM behavior disorder (a sleepdisorder) Mood disorders

Orthostatic hypotension (low bloodpressure when standing up)

Parkinson plus syndrome: Key


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Parkinson-plus syndrome: Key

features

Multiple system atrophy Parkinsonism, Cerebellar sign, Autonomic dysfunction

Progressive supranuclear palsy Parkinsonism, vertical gaze palsy

Corticobasal degeneration Parkinsonism, limb apraxia

Dementia with lewy bodies Parkinsonism, visual hallucination, fluctuation of

consciousness, dementia


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Drug induced parkinsonism


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Drug induced parkinsonism

Cause: dopamine receptor blocking drug Common: typical neuroleptic antipsychotic drug,

antidopaminergic antiemetic, reserpine (decreasepresynaptic)

Uncommon: SSRIs, lithium, phenytoin, methyldopa,valproic acid, flunarizine

Sign: symmetrical

postural tremor present

May up to 6 months after stop medication


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Common diseases

Tremor


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Tremor

a rhythmic oscillation of a body partproduced by alternating or synchronous

contraction of opposing muscles

other movement clinical symptoms can be act liketremor: dystonic tremor, myoclonic tremor


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Step app roach- MDS consensus

1. Inspection the tremor

2. Specific examination for assessment ofsigns related to tremor

3. Syndrome classification of tremor

Terminology for tremor and the


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Terminology for tremor and thehierarchical relation of the terms as

indicated by the numbers


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Inspection

Frequency

Low (7 Hz)

Location

Head: chin, face, tongue,palate

Upper extremity: shoulder,elbow, wrist, fingers

Trunk Lower extremity: hip, knee,

ankle joint, toes

Specific examination for


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Specific examination forassessment of:

Akinesia/bradykinesia Muscle tone (including Froments sign for the upper

and lower extremity and coactivation sign forpsychogenic tremor)

Postural abnormalities Dystonia Cerebellar signs

Pyramidal signs

Neuropathic signs Systemic signs (thyrotoxicosis and so forth) Gait and stance (orthostatic tremor)

Syndrome classification of tremor


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Syndrome Activity Specific S/S

Additional

features Cause

Physiologic tremor Rest NoAnxiety

aggravated

Physiologic

response

Enhance

physiologic tremor Postural, KineticHyperthyroid,

tachycardia

Response to beta-

blocker

Hyperthyroid,

drugs

Essential tremor Postural, Kinetic NoResponse to

alcoholNo

Parkinsoniantremor

RestBradykinesia,

postural instability,

rigidity

Response to L-dopa

Neuro-degeneration

Cerebellar tremorPostural, kinetic,

intentionAtaxia

May plus with

other neurological

deficit

Various cause

affected cerebellar

pathway

Syndrome classification of tremor


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Essential tremor

Core criteria for identifying ET Bilateral action tremor of the hands and

forearms

Absence of other neurological signs, with theexception of the cogwheel phenomenon

May have isolated head tremor with noabnormal posture


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Essential tremor

Secondary criteria for identifying ET

Long duration (>3 years) Family history: reported in > 50% of the

patients

Beneficial response to ethanol


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Achimedes spiral


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Treatment ET

First line

Propranolol start at 10 mg x 3 => 240-320 mg/d Primidone

Second line

Gabapentin, topiramate, clozapine, long actingbenzodiazepine (clonazepam)


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Common diseases

Alzheimers disease and other dementia

syndromes

Definition Amnestic syndrome

P f d l f h i di


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Definition Profound loss of the episodic memory Dementia

Acquired and persistent compromisein multiple cognitive domains that aresevere enough to interfere with every

day functioning Delirium or acute confusional state (ACS)

Prominent deficits or fluctuations inattention processing

Mild cognitive impairment (MCI)

the transitional state between theni iv h n n rm l in


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NEJM 2004


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Is it pseudo-dementia?

Term applied to apparent cognitive impairment associatedwith psychiatric disorders, most often depression (50-100%).

Four criteria proposed by Caine (1981) for diagnosis

1) intellectual impairment in a patient with a primarypsychiatric disorder

2) features of impairment are similar to those seen in CNSdisorders

3) the cognitive deficits are reversible 4) there is no known neurological condition to account for

the presentation

Caine (1981)

Sign suggest pseudo-dementia


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Sign suggest pseudo dementia

depressed affect/mood

neurovegetative signs slow, aspontaneous, monotonous speech

long response latency frequent "I dont know" responses quick to give up, but persists with encouragement

disorientation impaired attention/distraction incomplete responses

Sign suggest pseudo-dementia


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Sign suggest pseudo dementia

forgetfulness - particular deficits in learning newinformation, although memory may be patchy

poor abstraction

typically make errors of omission, vs. errors of commission

awareness of cognitive difficulties may have concern over deficits - "Do I have Alzheimers?

See, I cant remember anything!"

if psychosis, delusions typically nihilistic, self-deprecatory,paranoid

no signs of aphasia, apraxia, or agnosia

greater similarity to subcortical dementias, such asParkinsons


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Cl ifi ti f d ti


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Classification of dementia

Based on caused Cerebral disorder (with or without extrapyramidal

feature) VS systemic disorder

Reversible-Arrestable VS irreversible disorder

Based on site

Cortical VS subcortical Anterior (frontal premoter cortex) VS posterior(parietal and temporal lobe)

Progressive


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gneurodegenerative disease

Alzheimers

disease

Non-Alzheimers

disease

Parkinsons plus

dementia syndrome- PD, PSP, MSA, CBD,DLB, FTD-PD

Other- Picks disease

- Huntingtons chorea- Hereditary ataxia

- Wilsons disease

hemorrhage


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Treatable-Arrestable dementia Infection

CJD and varient,HIV infection,PML,Neurosyphilis,

TB, fungus,protozoal,

Whippels

diaease

Vitamin deficiency Vitamin B12

deficiency

Endocrine and other organ failureHypothyroidismAdrenal insufficiency and Cushing

syndromeHypo- hyperparathyroidismOrgan failure

Renal failure, Liver failureToxic/ metabolicAlcoholic dementia , Drug medication and

narcotic, Heavy metal intoxication, Dialysis dementia, Organic toxin,

Porphyria

Treatable-Arrestable


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Treatable Arrestable

dementia

Tumor Brain tumor (primary or metastatic),

Paraneoplastic limbic encephalitis

Head trauma and diffuse brain damage Dementia pugilistica, Chronic subdural

hematoma, Post anoxia, Postencephalitis

Normal pressure hydrocephalus

L b l i


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Lab evaluation

AAN guideline (Knopman et al. 2001)

Routine screening

Vitamin B12

Hypothyroidism

Clinical suspicious Blood screening for syphilis

Others Genetic testing: Apo E genotype

CSF test: beta amyloid, tau, AD7C-NTP

L b l ti


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Lab evaluation

AAN guideline (Knopman et al. 2001)

Non-contrast CT brain or MRI scan inmost case Minimizing the risk of failing to detect a

potentially treatable disorder

Identifying comorbidity such as stroke orischemic change

NINCDS-ADRDA Criteria


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NINCDS ADRDA Criteria

for diagnosis AD

DEMENTIA established by clinical examination;confirmed by cognitive screening test(MMSE)

Deficit of TWO or MORE area of cognitive function Progressive worsening of memory and other cognitive

function

No disturbance of consciousness

Onset between ages 40 and 90, most often after age 65 Absence of systemic disorders or others brain diseases

that could account for the deficits and progression

Neurology, Vol. 34, pp 939-944


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Parkinsonian Dementia Syndrome


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y Degenerative disorder

Familial HD, neuroacanthocytosis, MJD, progressive subcorticalgliosis, familial FTD

Sporadic PD with dementia, Parkinson plus syndrome(PSP, CBD,

MSA subtype), Dementia with Lewy bodies(DLB)

Secondary parkinsonism Drug, vascular, NPH, Whipples disease

Inherited metabolic disorder Wilsons disease

Hallevorden-Spatz disease

Idiopathic basal ganglia calcification

PDD vs DLB1 year rule

Parkinsons disease dementia(PDD)


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( )

THE LANCET Neurology 2003

Parkinson Dementia Syndrome


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Parkinson Dementia Syndrome

D.S. Geldmacher Clin Geriatr Med20 (2004) 2743

Frontotemporal lobe


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p

dementia Group of neurodegenerative dementia ofvaried etiology, in which the frontal a/o

temporal lobes are relatively selectively

affected, even into later stages of thedisease, and are associated with varying

amount of subcortical pathology and

degeneration

Mistaken for a psychiatric disorder

associated with inappropriate social behavior early

affects those middle aged rather than the elder


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Clinical feature of FTD


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Common diseases

Seizure and Epilepsy



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Seizure: the clinical manifestation of an

abnormal and hypersynchronousdischarge of a population of corticalneurons

Epilepsy: a tendency toward recurrent seizures

unprovoked by systemic or neurologicinsults

Classification of


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Epilepsy/Seizure

International League Against Epilepsy (ILAE)classification systems.

Seizures (1981)

Based on clinical features and EEG findings.

Replaces old terms such as Grand Mal, Petit Mal,psychomotor.

Epilepsies and Epileptic Syndromes (1989) Epileptic disorders with similar signs, symptoms, prognosis

and response to treatment.

Important for choosing treatment options and counselingpatients regarding etiology, genetics and likely prognosis etc.

ILAE Cl ifi ti f S i


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ILAE Classification of Seizures

Partial (Focal) Seizures: Arise in a limited number of cortical neurones within

one hemisphere

Generalized Seizures: Appear to arise simultaneously in both hemispheres

Unclassifiable Seizures:

ILAE Classification of the Epilepsies and

Epileptic Syndromes:


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Epileptic Syndromes:

Focal Generalised Undetermined Special Syndromes

Idiopathic Symptomatic/Cryptogenic Idiopathic Symptomatic/Cryptogenice.g.

- Benign Rolandic

- Benign Occipital

e.g.

- TLE

- FLE

- PLE- OLE

e.g.

- Childhood Absence

- Juvenile Absence

- Juvenile Myoclonic- GTCS on awakening

e.g.

- West Syndrome.

- Lennox-Gastaut.


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Seizure vs Syncope


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Seizure vs Syncope

Bhidayasiri R. et al. Neurological differential diagnosis 2005

Epileptic vs Pseudoseizure


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p p

Bhidayasiri R. et al. Neurological differential diagnosis 2005


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Common diseases

Headache disorder

International Classification

f H d h Di d 2004


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of Headache Disorder-2004

International Classification

of

Headache Disorder 2004

http://ihs-classification.org

Part 1. The primary headaches

- Migraine, TTH, CH and otherTACs, and other primary

headache disorder

Part II. The secondaryheadaches

-Headache attributed to ....

Part III. Cranial neuralgias,central and primary facial painand other headaches

Patient presents withcomplaint of a headache Red flag signs
http://ihs-classification.org/http://ihs-classification.org/http://ihs-classification.org/http://ihs-classification.org/


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Critical first step:

Hx taking, physical exam

Red flag signs or

alarming signs

Meets criteria for primary

headache disorder?

Migraine

headache

Tension-type

headache

Cluster

headache

and other

TACs

Chronic daily

headache (CDH)

Investigation

Secondary

headache

disorder

Other (rare)

headache

disorder

(+)(-)

(+)

Abnormal neurologicalexamination

Focal neurologic s/sother than typical visual

or sensory aura


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Normal neurological

examination

Papilledema

Temporal

profile

Concurrent

event

Provoking

activityAge

Age> 50

Sudden onset

-SAH, ICH, masslesion (posteriorfossa)

Worsening

headache

-Mass lesion, SDH,

MOH

Pregnancy, postpartum

-Cerebral vein

thrombosis, carotid

dissection, pituitary

apoplexy

Headache with

cancer, HIV,

systemic illness

(fever, arteritis,

collagen vascular

disease)

Neck stiffness

Triggered by cough,

exertion or Valsava

-SAH, mass lesion

Worse in the

morning-IICP

Worse on

awakening

-Low CSF pressure

Criteria for diagnosis


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Migraine without aura Infrequent ETTH

ICHD-II Cephalalgia.2004Migraine with typical aura needs 2 attacks

In children, the attack may last 1-72 hours

g

The Classic Migraine =

Mi i ith


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Migraine with aura

Migraine management


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Migraine management

Patient communication and education

Life style change and avoid trigger factors

Acute headache management

Prophylactic headache management

Pharmacotherapy for acute migraine attack


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Non-specific

Acetaminophen,

NSAIDs

butalbital

caffeine,

opioids

neuroleptic

Pharmacotherapy for acute migraine attack

SpecificDihydroergotamineErgotamineTriptan

Concept for prophylactic treatment


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Rightdrug

Right

person

Right

dose

Preventive medication thatwas proven the efficacy

Consider patient profiles, and

co-morbidities

Titrate into the appropriated

dose

Rightduration

On the preventive therapylong enough


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Recommended

medication for

migraine

prevention EFNSguideline 2009

Evers, S et al.

European Journal of Neurology 2009, 16: 968981

Drugs Relative indicationsRelative

t i di tiAdverse effect

Indications, contraindications, and adverse effects of conventional migraine preventive drugs


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Drugs Relative indicationscontraindication

Adverse effect

Amytriptiline (TCA)

Propranolol (B-

blocker)

Flunarizine (CCB)

Valproic acid (AED)

Topiramate (AED)

Other pain disorders,

depression, anxiety,

insomnia

Hypertension, angina

Hypertension, vertigo

Epilepsy, mania,

anxiety

Epilepsy, mania,

anxiety

Mania, urinary

retention, heart blocks,

glaucoma

Asthma, depression,

CHF, Raynauds

disease

Obesity, depression,

PD

Liver disease, bleeding

disorder

Renal calculosis, liver

disease

Drowsiness, dry

mouth, increase

appetite, weight gain

Fatique, lethargy,

nausea, depression,

dizziness

Drowsiness, weight

gain, depression, PD

Nausea dyspepsia,

sedation, increase

appetite, weight gain

Paresthesia, weight

loss, alter taste,

language disturbance

F. Galletti et al. Progress in Neurobiology 89 (2009) 176192


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