Psychiatry tutorial

Surat Tanprawate, MD, FRCP(T) Division of Neurology, Chiang Mai University 11.05.2013

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: Alzhermer’s disease, Huntington’s disease, etc.

• Psychiatric consequence of neurological disease: post-stroke depression
• Functional symptoms in neurology

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

Mood and affect lability
Clinical symptoms/syndro mes

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

Pseudobulbar palsy
Balbar: LatinBulb: A globular or fusiform anatomical structure or enlargement.Bulbus: swollen root

Bulbar palsy refers to bilateral impairment of function of the cranial V, VII, IX, X and XI, which occurs due to lower motor neuron lesion either at nuclear or fascicular level in the medullar oblongata or from bilateral lesions of the lower cranial nerves outside the brainstem

The Brainstem

Pseudobulbar palsy
Pseudobulbar palsy results from an upper motor neuron lesion to the corticobulbar pathway in the pyramidal tract.
Symptoms: -difficulty chewing, swallowing -slurred speech (often initial presentation) -inappropriate emotional outbursts.

“Pathological laughing and crying”

Pathological Laughter

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Pathological crying

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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

Epileptic seizure
• A gelastic seizure • sudden burst of energy, usually in the form of laughing or crying • Cause: hypothalamic hamartomas, temporal and frontal lobe lesion

• Frontal lobe and temporal lobe epilepsy

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

Hallucination and illusion
Clinical symptoms/syndro mes

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

Visual pathway
Eye

Occipital cortex

Optic nerves

Temporal lobe

Geniculocalcarin e projections

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 lesions result in an inappropriate pattern of cortical excitation

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

Common causes of complex visual hallucination
• Migraine aura • Epilepsy • Charles- Bonnet syndrome • Peduncular hallucinosis • Treated idiopathic Parkinson’s diseaseLewy body dementiaNarcolepsy-cataplexy syndromeSchizophreniaDelirium

Hallucination of the cerebral cortex
• Destructive lesion: “release hallucination” • Neuronal hyperexcitability: “migraine” and “epileptic seizure”

A 37 Y.O. man with abnormal visual symptoms for 2 weeks
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“Release hallucination from temporo-occipital lobe infarct”

Migraine Aura
99% 31%

Typical aura: -Visual -Sensory -Speech
6%

18%

n=163
Michael B. R. et al. Brain 1996: 119, 355-361

Typical aura
• Typical aura consisting of visual and/or sensory and/or speech symptoms. Gradual development, duration no longer than one hour, 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 without aura.

Visual aura

Typical visual aura is simple

Alice in Wonderland Syndrome (AWS)

Somesthetic metamorphopsia. Distortion of body and spaceDid Lewis Carroll draw inspiration from migraine auras?
Alice in Wonderland. By Lewis Carroll

Blindness, visual hallucination and Charles Bonnet syndrome(CBS)

The disease is named after the Swiss philosopher, who described the condition in 1769.

He first documented it in his 89-year-old grandfather who was nearly blind from cataract in both eyes but perceived men, women, birds, carriages, buildings, tapestries, physically-impossible circumstances and scaffolding patterns.

Charles Bonnet, Swiss philosopher who described CBS in 1760

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

Peduncular hallucinosis “Hallucination of the midbrain”

Described a 72-year-old woman’s visual hallucination of colorfully dressed people and children which occurred at dusk. The hallucinations occurred during normal conscious state and the patient’s neurological signs were associated with those characteristic of an infarct to the midbrain and pons. Von Bogaert, Lhermitte’s colleague, named these type of hallucinations “peduncular” in reference to the cerebral peduncle as well as to the midbrain and its surroundings.

Lhermitte French neurologist

Visual hallucination with Parkinsonism
• 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(Parkinson’s disease) and atypical parkinsonism

Visual hallucination with Parkinsonism
• Parkinson’s 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

Comparison of DLB with AD and PD

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

Visual hallucination 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

Visual hallucination in schizophrenia
Schizophrenia
• Animals and figures may be prominent
• Usually in colour

Organic cause

less paranoid and thought disorder more insight associated with abnormal physical signs/symptoms more often nocturnal, and are associated with drowsiness

• • •

• with auditory hallucination
• occur throughout working hours

Complex visual hallucination in focal epilepsy

• usually brief, sterotyped and fragmentary

• associated with other seizure manifestation
• Strong evidence: EEG recording

Disorder of consciousness
Clinical symptoms/syndrom es

Arousal and awareness, the two components of consciousness in coma, vegetative state, minimally conscious state, and locked-in syndrome.

Behavioral state confused with coma
Behavioral state
Locked-in syndrome

Definition
Alert and aware, quadriplegic with lower CN palsy

Lesion
Bilateral anterior pontine

Comment
Similar state:severe polyneuropathy MG, NM blocking agent

Persistent vegetative state

Absent cognitive function but retain vegetative component

Extensive cortical grey Synonyms include apallic and subcortical white syndrome, coma vigil, matter with relative cerebral cortical death preservation of brain stem

Abulia

Severe apathy, patient neither Bilateral frontal medial speak nor moves spontaneously

Severe case resemble akinetic mutism, but patient is alert and aware

Catatonia

Mute, and mark decrease motor activity

Usually psychiatric

May be mimicked by frontal lobe dysfunction and drug

Pseudocoma

Feigned coma

Locked in syndrome

Disorders of Diminished Motivation
Akinetic mutism

Apathy
• DDx

Abulia

• 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

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

Conditions associated with apathy, abulia, and akinetic mutism

Robert S. Marin,. J Head Trauma Rehabil.2005: 4(20)377388

Frontal Lobe Syndrome
Clinical symptoms/syndrom es

Phineas P. Gage

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Phineas P. Gage (1823 –1860) was an American railroad construction foreman now remembered for surviving an accident in which a large iron rod was driven completely through his head, destroying much of his brain's left frontal.

Prefrontal cortex
• 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

General organization of the frontal-subcortical circuits

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

3 distinct cortical subcortical circuit

Organization of the three frontal-subcortical circuits in which lesions produce alterations of cognition and emotion. VA indicates ventral anterior; MD, medial dorsal.
Cummings JL. Arch Neurol. 1993;50:873-880

Symptoms of frontal lobe dysfunction

Anterior cingulate gyrus
aphathy

Orbitofrontal cortex
disinhibition anosmia

Symptoms of frontal lobe dysfunction

Executive function planning, initiating,
sequencing(maintaining, alternating, stopping), and monitoring behavior •Executive dysfunction poor strategies including impaired planning when copying constructions and when organizing material to be remembered • impaired set shifting in response to changing task contingencies • abnormalities of motor programming • compromised attention

Aphasia
Clinical symptoms/syndrom es

Aphasia
• Aphasia refers to an impairment in linguistic communication produced by brain dysfunction

• It must be distinguished from other disorders of verbal output such as dysarthria, mutism, and the abnormal language production of patients with thought disorder

Language test
• Speech fluency
• Comprehension • Repetition • Naming

• Writing

transcortical motor aphasia

Transcortical sensory aphasia

Motor aphasia

Sensory aphasia

A: Wernicke's area B: 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.

Conduction aphasia

Articulatory disorder (aphemia)

Pure word deafness

Lichtheim's diagram of the language system

Aphasia chart

Broca’s aphasia

Pierre Paul Broca (1824 –1880) French physician

• 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

Wernicke’s aphasia

Carl Wernicke (1848-1905)
German physician, psychiatrist, neuropathologist

• 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.

Common neurological diseases
Alzheimer’s disease and dementia syndromes
Parkinson’s disease and other Parkinsonism Headache disorders

Parkinson’s disease and other Parkinsonism
Common diseases

James Parkinson, London (1755 – 1824)

An Essay on the Shaking Palsy(1817)
Shaking Palsy(Paralysis agitans)

He identified 6 cases, 3 of whom he personally examined; 3 he observed on the streets of London
J Neuropsychiatry Clin Neurosci 2002;14:223–36

Stooped posture

Paralysis agitan (shaking palsy)

Rigidity

Tremor

Reduce arm swing Hips and knees slightly flex Short shuffling steps

• •

Parkinsonism

• •

clinical syndrome of bradykinesia, resting tremor, cogwheel rigidity, and postural instability

Parkinson’s 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-laden dopaminergic neurons containing eosinophilic cytoplasmic inclusions(Lewy bodies)

Something look alike
• Gait disorder • Tremor: severe essential tremor,
cerebellar tremor

• Depression • Psychomotor retardation • Frontal lobe syndrome

• Primary or idiopathic parkinsonism •Group Parkinson’sof disease Parkinsonism • Secondary parkinsonism TYPICAL OR • hydrocephalus, vascular CLASSIC
parkinsonism, encephalitis, drug induced parkinsonism

• Parkinson plus syndrome • Progressive supranuclear
palsy(PSP), corticobasal degeneration(CBD), multiple system ATYPICAL atrophy(MSA), Dementia of Lewy Bodies(DLB)

• Hereditary parkinsonism

Parkinson’s disease

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

PD- diagnostic criteria

Diagnostic accuracy to 82%
Gibb et al, 1988, Table from Litvan et al, 2003

Non-motor symptoms
• Loss of sense of smell, constipation • REM behavior disorder (a sleep
disorder)

• Mood disorders • Orthostatic hypotension (low blood
pressure when standing up)


• • •

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

Drug induced parkinsonism

Cause: dopamine receptor blocking drug

• •

Common: typical neuroleptic antipsychotic drug, antidopaminergic antiemetic, reserpine (decrease presynaptic) Uncommon: SSRIs, lithium, phenytoin, methyldopa, valproic acid, flunarizine

• •

Sign:

• •

symmetrical postural tremor present

May up to 6 months after stop medication

Tremor
Common diseases

Tremor
• a rhythmic oscillation of a body part
produced by alternating or synchronous contraction of opposing muscles

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

Step approach- MDS consensus
1. Inspection the tremor

2. Specific examination for assessment of signs related to tremor
3. Syndrome classification of tremor

Terminology for tremor and the hierarchical relation of the terms as indicated by the numbers

Inspection

Frequency

• Location
• • • •
Head: chin, face, tongue, palate Upper extremity: shoulder, elbow, wrist, fingers Trunk Lower extremity: hip, knee, ankle joint, toes

• • •

Low (<4 Hz) Medium (4-7 Hz) High (>7 Hz)

Specific examination for assessment of:
• • • • • • • • •
Akinesia/bradykinesia Muscle tone (including Froment’s sign for the upper and lower extremity and coactivation sign for psychogenic 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
Syndrome Activity Specific S/S
Additional features

Cause Physiologic response
Hyperthyroid, drugs

Physiologic tremor

Rest

No

Anxiety aggravated
Response to betablocker

Enhance physiologic tremor

Postural, Kinetic

Hyperthyroid, tachycardia

Essential tremor

Postural, Kinetic

No Bradykinesia, postural instability, rigidity

Response to alcohol Response to Ldopa

No

Parkinsonian tremor

Rest

Neurodegeneration

Cerebellar tremor

Postural, kinetic, intention

Ataxia

May plus with Various cause other neurological affected cerebellar deficit pathway

Essential tremor
• • • •
Core criteria for identifying ET Bilateral action tremor of the hands and forearms Absence of other neurological signs, with the exception of the cogwheel phenomenon May have isolated head tremor with no abnormal posture

Essential tremor

Secondary criteria for identifying ET

• •

Long duration (>3 years)
Family history: reported in > 50% of the patients Beneficial response to ethanol

Achimedes spiral

Treatment ET
• First line
• •

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

• Second line
Gabapentin, topiramate, clozapine, long acting benzodiazepine (clonazepam)

Alzheimer’s disease and other dementia syndromes
Common diseases

Amnestic syndrome

Definition • Profound loss of the episodic memory
Dementia

• Acquired and persistent compromise
in multiple cognitive domains that are severe enough to interfere with every day functioning
Delirium or acute confusional state (ACS)

• •

• Prominent deficits or fluctuations in
attention processing
Mild cognitive impairment (MCI)

• the transitional state between the
cognitive changes of normal aging

NEJM 2004

Is it pseudo-dementia?

Term applied to apparent cognitive impairment associated with psychiatric disorders, most often depression (50-100%). Four criteria proposed by Caine (1981) for diagnosis

• • • •

1) intellectual impairment in a patient with a primary psychiatric disorder 2) features of impairment are similar to those seen in CNS disorders 3) the cognitive deficits are reversible 4) there is no known neurological condition to account for the presentation Caine (1981)

Sign suggest pseudo-dementia

• • • • • • • • •

depressed affect/mood neurovegetative signs slow, aspontaneous, monotonous speech long response latency frequent "I don’t know" responses

quick to give up, but persists with encouragement
disorientation impaired attention/distraction incomplete responses

Sign suggest pseudo-dementia
• • • • • • • •
forgetfulness - particular deficits in learning new information, 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 Alzheimer’s? See, I can’t remember anything!" if psychosis, delusions typically nihilistic, self-deprecatory, paranoid no signs of aphasia, apraxia, or agnosia greater similarity to subcortical dementias, such as Parkinson’s

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 neurodegenerative disease
Alzheimer’s disease Non-Alzheimer’s disease

Parkinson’s plus dementia syndrome
- PD, PSP, MSA, CBD, DLB, FTD-PD

Other
- Pick’s disease - Huntington’s chorea - Hereditary ataxia - Wilson’s disease

• Infarction,

• Infection Treatable-Arrestable dementia • CJD and varient,
HIV infection, PML, Neurosyphilis, TB, fungus, protozoal, Whippel’s diaease

hemorrhage

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

• Vitamin deficiency • Vitamin B12
deficiency

• • •

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, Post encephalitis

Normal pressure hydrocephalus

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

Lab evaluation
• AAN guideline (Knopman et al. 2001) • Non-contrast CT brain or MRI scan in
most case


Minimizing the risk of failing to detect a potentially treatable disorder
Identifying comorbidity such as stroke or ischemic change

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

Parkinsonian Dementia Syndrome

Degenerative disorder

• Familial

HD, neuroacanthocytosis, MJD, progressive subcortical gliosis, familial FTD

• Sporadic

PD with dementia, Parkinson plus syndrome(PSP, CBD, MSA subtype), Dementia with Lewy bodies(DLB)

• •

Secondary parkinsonism

• • • •

Drug, vascular, NPH, Whipple’s disease

Inherited metabolic disorder
Wilson’s disease Hallevorden-Spatz disease Idiopathic basal ganglia calcification

PDD vs DLB 1 year rule

Parkinson’s disease dementia(PDD)

THE LANCET Neurology 2003

Parkinson Dementia Syndrome

D.S. Geldmacher Clin Geriatr Med 20 (2004) 27–43

Frontotemporal lobe dementia

Group of neurodegenerative dementia of varied etiology, in which the frontal a/o temporal lobes are relatively selectively affected, even into later stages of the disease, 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

Clinical feature of FTD

Seizure and Epilepsy
Common diseases

Seizure and Epilepsy

Seizure:

the clinical manifestation of an abnormal and hypersynchronous discharge of a population of cortical neurons

Epilepsy:

a tendency toward recurrent seizures unprovoked by systemic or neurologic insults

Classification of 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 counseling patients regarding etiology, genetics and likely prognosis etc.

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:

Focal

Generalised

Undetermined

Special Syndromes

Idiopathic

Symptomatic/Cryptogenic
e.g. - TLE - FLE - PLE - OLE

e.g. - Benign Rolandic - Benign Occipital

e.g. - Childhood Absence - Juvenile Absence - Juvenile Myoclonic - GTCS on awakening

Idiopathic

Symptomatic/Cryptogenic e.g. - West Syndrome. - Lennox-Gastaut.

Absence vs CPS

Bhidayasiri R. et al. Neurological differential diagnosis 2005

Seizure vs Syncope

Bhidayasiri R. et al. Neurological differential diagnosis 2005

Epileptic vs Pseudoseizure

Bhidayasiri R. et al. Neurological differential diagnosis 2005

Headache disorder
Common diseases

International Classification of Headache Disorder-2004
Part 1. The primary headaches - Migraine, TTH, CH and other TACs, and other primary headache disorder Part II. The secondary headaches
International Classification of Headache Disorder 2004

-Headache attributed to ....
Part III. Cranial neuralgias, central and primary facial pain and other headaches

http://ihs-classification.org

Patient presents with complaint of a headache

Red flag signs
(+)

Critical first step: Hx taking, physical exam

Investigation

Red flag signs or alarming signs

Meets criteria for primary headache disorder?

(-)

(+)

Migraine headache
Cluster headache and other TACs

Tension-type headache Chronic daily headache (CDH)

Other (rare) headache disorder

Secondary headache disorder

Abnormal neurological examination Normal neurological examination
Age

Focal neurologic s/s other than typical visual or sensory aura Papilledema Neck stiffness

Temporal profile
Worsening headache -Mass lesion, SDH, MOH

Concurrent event
Pregnancy, post partum -Cerebral vein thrombosis, carotid dissection, pituitary apoplexy Headache with cancer, HIV, systemic illness (fever, arteritis, collagen vascular disease)

Provoking activity
Triggered by cough, exertion or Valsava -SAH, mass lesion

Age> 50

Sudden onset -SAH, ICH, mass lesion (posterior fossa)

Worse in the morning -IICP

Worse on awakening -Low CSF pressure

Criteria for diagnosis
Migraine without aura Infrequent ETTH

Migraine with typical aura needs 2 attacks In children, the attack may last 1-72 hours

ICHD-II Cephalalgia.2004

The “Classic” Migraine = Migraine with aura

Migraine management
• Patient communication and education
• Life style change and avoid trigger factors • Acute headache management • Prophylactic headache management

Pharmacotherapy for acute migraine attack
• Non-specific
• Acetaminophen, • NSAIDs • butalbital • caffeine, • opioids

• Specific DihydroergotamineErg otamineTriptan

• neuroleptic

Concept for prophylactic treatment
Right drug Right person Right dose
Right duration
Preventive medication that was proven the efficacy Consider patient profiles, and co-morbidities Titrate into the appropriated dose
On the preventive therapy long enough

Recommended medication for migraine prevention “EFNS guideline 2009”

Evers, S et al. European Journal of Neurology 2009, 16: 968–981

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

Drugs
Amytriptiline (TCA)

Relative indications

Relative contraindication

Adverse effect

Other pain disorders, Mania, urinary Drowsiness, dry depression, anxiety, retention, heart blocks, mouth, increase insomnia glaucoma appetite, weight gain

Propranolol (Bblocker)

Hypertension, angina

Asthma, depression, CHF, Raynaud’s disease Obesity, depression, PD Liver disease, bleeding disorder

Fatique, lethargy, nausea, depression, dizziness Drowsiness, weight gain, depression, PD Nausea dyspepsia, sedation, increase appetite, weight gain Paresthesia, weight loss, alter taste, language disturbance

Hypertension, vertigo Flunarizine (CCB) Epilepsy, mania, anxiety

Valproic acid (AED)

Topiramate (AED)

Epilepsy, mania, anxiety

Renal calculosis, liver disease

F. Galletti et al. Progress in Neurobiology 89 (2009) 176–192

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