Lecture notes Neurological And Psychiatric Disorders (AB_1023)

Lectures NPD

Lecture 1: Brain Imaging
- Understand application/possibilities of neuroimaging in clinic and research
o Clinic
 Diagnosis/prognosis
 CVA
 CT/MRI/MRS/angiography/X-ray
 CT fast acute conditions
o Research
 Improve diagnostics
 Prediction
 Post-mortem MRI & histopathology
 Understand biological processes (using advanced imaging techniques)
 Qualitative
 Standard clinical practice  eg MS
 Look for pathology
 Quantitative
 “numbers as output
 Understand biological mechanisms
 Compare patient groups to healthy controls
 Structural MRI
o Brain volumes (atrophy)
o White matter integrity diffusion tensor imaging
 Functional MRI
o Brain activation during cognitive/motor task
o Functional connectivity
- Recognize abnormalities on brain scans & understand their underlying pathology
o Hemorrhage
 Epidural hematoma between dura mater & skull
 Acute (trauma) CT
 Lens-shaped
 Symptoms delayed
o Loss of consciousness disappears
o Progressive headache
o Nausea
o Fluid (cerebrospinal fluid) draining from nose/ears
 Arteries
 Tissue pushed inside
 Subdural hematoma between dura mater and arachnoid
 More often than epidural
 Bridging veins
 Slow buildup of blood
 3 types
o Acute <24 h (worst prognosis)
o Subacute <10 days
o Chronic >10 days
 Midline shift
 Intercranial pressure consciousness decreases; stiff pupil
 Intracerebral hematoma
o Herniation occurs when something inside the skull produces pressure that moves the
brain tissues
 Different types
o Hypertension

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, o Aneurysm
 Thin wall of blood vessel
 Balloon forms (aneurysm)
 Aneurysm pops bleeds
 Balloon is clipped off
o Arteriovenous malformation (AVM)
 Asymptomatic or headaches/epilepsy
 Arteries and veins not connected correctly
 Conventional T2 SE MRI
 TOF-MRA (MIP reconstruction
o Intracerebral/intraparenchymal hemorrhage
o Stroke
 CT darker
 MRI white
 MRA decrease in blood flow
o Brain tumor
 T2 weighted MRI white
- Understand application of different MRI sequences/techniques in MS
o MRI magnetic resonance imaging
 Uses magnetism and radiofrequency signals to acquire images
 50,000 times more powerful than magnetic field of earth
 Conventional MRI sequences
 T1-weighted scan
o Contrast fat/water
o Anatomy
 T2-weighted scan
o Contrast water/tissue (T tWo water=white)
o pathology
o MS lesions
 T2 bright white spots
 Advantages
 Highly sensitive in detection of lesions
 Reflects disease duration
 Disadvantages
 Lack of histopathological specificity
 Moderate correlation with clinical disability clinic-radiological paradox
o Acute inflammation  white (old lesions dark)
 Disruption BBB
 Acute inflammation 2-8 weeks
 May coincide with relapse
 Intravenous gadolinium
 T1 weighted images
 Best seen 15-30 min p.i.
 “black holes” (letterlijk op T1 scan) disease severity (no remyelination)
o Typical locations
 Juxtacortical
 Corpus callosum
o Cortical lesion detection
 Double inversion recovery (DIR)
o T2 scan
 Number of lesions on baseline MRI predicts
 Conversion to clinically definite MS
 Development of new lesions
 Development of mild to moderate disability

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,Lecture 2: Clinical aspects of depression
- Classification of unipolar depressive disorders DSM-V
o Major Depressive Disorder  2 weeks
o Persistent Depressive Disorder  2 years
o Symptoms  5/9 for at least 2 weeks (including core symptoms)  many different
combinations
 Depressed mood
 Loss of interest or pleasure in activities
 Changes in weights or appetite
 Insomnia or hypersomnia
 Psychomotor agitation/retardation
 Fatigue
 Feelings of guilt/self-reproach
 Concentration problems
 Suicidal thought
- Prevalence rates
o US
 18-25
 Women>men
 Difference in ethnicity
o NL
 Women> men
 Lower prevalence than US
 No data > 65 years old
 Lifetime & 12-month prevalence
 Lifetime ¼ women
 12-month ±5%
 65+ (LASA)
 Depressive symptoms higher percentage
o Depends on setting
 Urban> rural
 Higher in population with somatic problems
o Average age of onset mid 20s
 Duration
 Average: 4-6 months
 50% over 1 year
 10-20% persistent or chronic depression influences prevalence rates
 Recurrence
 50% has recurrent episodes
 After 2nd or 3rd episode risk for recurrence 70% or 90%
- High societal burden, but undertreatment
o Years lived with disability (YLD)
 Prevalence * loss of health (disability weight)
o Disability Adjusted Life Years
 YLD + years of life lost (YLL)
o YLS & DALYs increased in the last decades
o 2020 depression is expected to be the second leading cause of disability
 But: of 80/1000 depressed people, who consult GP, 49 are not recognized as
depressed
 If recognized ¼ / 1/5 are referred to secondary mental health services
- Pathophysiology
o Complex many factors
o Etiology  epigenetics

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,  Genetics
 G1/G2/G3 etc.
 Environment
 Stress/trauma/interpersonal dynamics etc
o Pathophysiology all interact with each other  strong/medium evidence
 Neurotransmitters 5-HT/NE/DA/Glu
 Inflammation
 HPA axis hyperactivity
 Reduced neuroplasticity
 PFC-limbic altered connectivity
o Clinical phenotype
 Domains
 Negative salience
 Reward sensitivity
 Motor activity
 Impulsivity
 Sleep/arousal
 Symptoms
 Sadness/guilt
 Anhedonia
 Psychomotor agitation/retardation
 Suicidality
 sleeplessness
o Recurrence Neuroprogressive nature of major depressive disorder
 Medication continuation




o Connectivity problems areas not reached well
 Hypoconnectivity Frontoparietal Network cognitive control & attentions &
emotion regulation
 Hyperconnectivity Default Network internally oriented and self-referential
thought
 Hypoconnectivity Affective Network processing emotions or salience
- Treatment
o Antidepressants help with higher Hamilton scores  then there is a difference between
placebo and real medication
 Don’t give everybody medication
o Guidelines

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