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Basic mechanisms of nervous system diseases > kyssärei > Flashcards

kyssärei Flashcards

1
Q

Non-motor symptoms in Parkinson’s disease?

A 
AUTONOMIC
- postural (orthostatic) hypotension
- constipation, dysphagia 
- urinary frequency/urge
- impotence
- hyperhidrosis
MOOD, COGNITION,
BEHAVIOR
- depression, apathy, anxiety
- compulsive behavior
- hallucinations, psychosis
- deficits in attention/memory
- dementia (in 30%)
SENSORY
- impaired sense of smell
- pain
- numbness, tingling
-(visual disturbances?)
SLEEP-WAKE
- excessive daytime sleepiness
- restless legs
- insomnia, sleep fragmentation
- REM sleep behavior disorder 
- sleep apnea
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2
Q

What dysfunction happens in gastrointestinal in parkinson’s disease?

A 
Mouth:
-pooling of saliva
-problems with movements needed to brush teeth
-Jaw tremors
Oesophagus (ruokatorvi)
-slow transit
-spontaneous contractions
-air trapping
Small intestine
-dilatation
Colon
-Colonic dysmotility
-Constipation
-Megacolon
Salivary Glands
-reduced saliva production
-Low swallowing frequency causes drooling
Pharynx(nielu)
-oropharyngeal dysphagia increases risk of aspiration
Stomach:
-Impaired gastric emptying->nausea, weight loss
Rectum
-anorectal dysfunction leads to difficulity with defecation
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3
Q

What are the main diseases that cause dementia?

A

Alzheimer, Vascular dementia, Dementia with lewy bodies, Frontotemporal dementia, Other diseases

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4
Q

What is the prevalence of dementia?

A

Age from 86 to 90 the prevalence is ~40% and under 72 years ~4%

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5
Q

What supports the fact that PD starts from the gut?

A

-alpha-synuclein expressed in human enteric NS correlates with intestial inflammation and implicates common GI infections in pathogenesis of PD
-correlates with REM sleep behavior
- Gut microbiota alterations in PD have been consistently described and linked to
alterations in metabolism, inflammatory cytokines, symptoms, and disease
progression.

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6
Q

support for calcium hypothesis in AD:

A
  • calsium modulates many nauronal prosees, synaptic plasticity and apoptosis
    • dysregulation of intracellular calcium signaling has implicated pathogeneisis of AD
    • increased intracellular calsium->lesions of this disorder like accumulation of amyloid-beta, hyperphosphorylation of TAU and neuronal death
    • Every gene that is known to increase susceptibility of AD also modulates some aspect og calcium signalling
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7
Q

support for Amyloid hypothesis in AD:

A
  • autosomal dominant forms of AD create mutations in APP
  • Trisomy 21 all develop AD-like pathology (APP in gene 21)
  • ApoE4 have increased A-b42 depositions
  • Plaques
  • Rats that overexpress AB can have cognitive deficits reversed by antibodies against AB oligomers
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8
Q

support for Tau hypothesis in AD:

A
  • sufficient to cause a neurogenerative illness
  • some persons with extensive plaques are not demented
  • tau kinase GSK3 processes beta amyloid plaques as well
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9
Q

Support for cholinergic hypothesis in AD:

A
  • strong relationship between neurotransmission and cognitive functions
    • ACh important for learning and memory
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10
Q

Pathological features of AD:

A
  • Neuronal loss in cortex and hippocampus
  • Deposition of beta amyloid (Aß)
  • Presence of intraneuronal neurofibrillary tangles TAU
  • Oxidative stress
  • Mitochonrial dysfunction
  • Calcium imbalance
  • Hormonal dysregulation
  • Inflammatory response
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11
Q

Role of microglia in general and in AD?

A

Microglia has multiple roles in the brain throughout life such as prune synapses, assist myelination, contribute in neurogeneration

-disease associated microglia (DAM) -> activated by TREM2- independent and dependent pathways in AD

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12
Q

Effect of astrocytes and microglia in early and late stage of AD:

A

In early stage: atrophic astrocyte-> reduced synaptic coverage, dysfunction in neuro-vascular unit, reduced bloodflow, reduced metabolic support, altered extracellular homeostasis of ions and neurotransmitters->reduced synaptic connections and synaptic loss—> cognitive deficits

In late stage: Plaque->reactive astrocyte and microglia activation(release of inflammatory and neurotoxic factors and failure in homeostasis->neuronal death->cognitive deficits- also >brain atrophy

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13
Q

Role of microglia in general?

A

Microglia has multiple roles in the brain throughout life such as prune synapses, assist myelination, contribute in neurogeneration

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14
Q

Is vascular dementia small vessel disease?

A

Yes it is: diffuse changes and lacunar infarcts (most common type of ischaemic stroke resulted from occlusion of small penetrating arteries )

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15
Q

Is pure vascular dementia rare?

A

Yes! these vascular changes are often accompany neurodegenerative disorders (mixed dementia)

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16
Q

Pathological mechanism identified in ALS?

A

xidative stress, Mitochondrial defects, Axonal transport impairment, neuroinflammation, protein misfolding, RNA dysregulation etc..

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17
Q

Genes in migraine?

A

CACNA1A, ATP1A2, SCN1A, PRRT2 in familial migraine

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18
Q

What is organization of skeletal muscle?

A

Epimysium, Perimysium,

Endomysium

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19
Q

How is depression diagnosed?

A

Major depressive disorder DSM:
A) five (or more) of following symtoms during a 2-week period, 1 is depressed mood or loss of interest/plesure
depressed mood most of the day, every day
diminished interest or pleasure in all activities every day
weight loss when not dieting or weight gain
Insomnia or hypersomnia nearly every day
psychomotor agitation or retardation nearly every day (levottomuus ja hidastuminen?)
fatigue and loss of energy
diminished ability to think and concentrate
thoughts of death and suicide
feeling of worthlessness or guilt

B) the symptoms cause significant distress or impairment in social, occupational or other important areas of functioning

C) The episode is not attributable to other physiological effects of a substance or to another medical condition

D) can’t be explained better by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder or other psychotic disorders

E)there has never been manic episode or a hypomanic episode

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20
Q

Important brain areas in neural circuits in depression?

A
  • dorsal anterior cingulate(dACC)
  • dorsomedial prefrontal cortex,
  • ventromedial prefrontal cortex,
  • bilateral anterior insula
  • thalamus
  • amygdala
  • hippocampus
  • superior temporal gyrus
  • parietal operculum
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21
Q

Treatment methods for depression?

A
  • DBS
  • TMS
  • Antidepressant medication (works slowly)
  • Neurotrophic factors
  • SSRI(selective serotonin reuptake inhibitors)
  • Medications such as: sleeping pills, pain relievers, cortisone drugs…
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22
Q

Which disease are these genes associated with:

DRD2, GRM3, SPR, GRIA1, CACNA1C, CACNB2, CACA1I, CSMD1, 22q11DS and what do they regulate?

A

Schizophrenia:
75% of gene encoding for protein:
-Dopamine-2-receptor (DRD2), -genes incolved in glutamate transmission(GRM3, GRIN2A, SPR, GRIA1),
-Ca-channel genes(CACNA1C, CACNB2, CACA1I)
-CSMD1, encoding a regulator of C4 (promote synapse elimination during development in mice), also associates to SZ

  • 22q11DS (velocardiofacial-DiGeorge syndrome)
    • about 1-2% of patients with SZ
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23
Q

Treatment of SZ?

A
  • antipsychotic medication
    • psychosocial treatment
    • psychosocial rehabilitation
    • psychoeducation of the patient and the family
    • occupational rehabilitation
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24
Q

Basic mechanisms in SZ?

Epigenetic mechanisms for SZ?

A
  • something to do with dopamine increasing? also norepinephere, serotonin and GABA involved, much unknown
  • Cortical thinning, correlated with severity of symtoms
  • Decreament in synaptic spines
  • Brain circuit abnormalities (changes in these circuits, particular in PCX, HC, thalamus and striatum)
  • Extensive epigenetic programming during development
  • 1)dysregulation of GABAergic system in SZ
    • decrease of GAD67 (enzyme involved in synthesis of GABA) or other ways affects
  • 2) deviated microRNA regulation
    • associated in rs1625579
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25
Q

Risk factors of MS?

A

Genetic factors:

  • antigen presentation
  • T-lymphocyte apoptosis
  • T-lymphocyte proliferation
  • Cell adhesion
  • Lymphocyte development

Environmental:

  • Epstein-Barr Virus (EBV) and maybe other herpesviruses
  • Lack of UV light in childhood
  • Lack of vitamin D
  • Smoking
  • organic solvents
  • teenage obesity

Early development:
Mont of birth effect
-T-cell development
-Lack of D-vitamin

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26
Q

How is MS diagnosed?

A
  • T-cell composition in acute MS plaque
  • Symptoms and neurological signs compatible with MS.
  • Optic neuritis (visual evoked potential)
  • Sensory or motor paresis
  • Brain stem syndrome
  • Spinal syndrome
  • MRI for brain and spinal cord
  • CSF: intrathecal antibody
  • Exclusion of infections and other causes
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27
Q

Symptoms in MS, different areas of the body?

A

Cerebral hemisphere:

  • muscle weakness
  • sensory symptoms
  • optic neurites->involuntery rapid eye movements, loss of vision

Brain stem:

  • Paresis of limbs or face
  • hearing loss
  • vertigo
  • eye muscle pareses
  • mouth, tongue, throat pareses

Spinal cord:

  • Pareses
  • sensory symptoms (pain sensed in skin)
  • ataxia(loss of nerve cells)
  • problems with urinary/bladder, sex functions

Cerebellum:

  • vertigo
  • ataxia
  • speach:dysarthria
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28
Q

Treatment of MS? What should be focused in future?

A
  • Lowering body temperature
  • For urinary incontinence: training mucles, botox in bladder walls, anticholinergic drugs, cathererisation
  • For neuropathic pain: epilepsy and depression drugs
  • cognitive rehabilition therapy
  • D vitamin?
  • physical therapy
  • Disease modifying drugs: Immunomodulation, migration inhibition, cytotoxity

In future: focus on identification of the driven cell types

  • T-cell receptor clonotyping and single-cell transriptome analysis
  • Analysis of EBV-memory cells
  • Is EBV really present in MS-plaque?
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29
Q

Risk factors for dementia? Who may be affected?

A
  • age: elderly people (only under 4% under 75)
  • smoking
  • diabetes
  • having one of the causing diseases
  • vascular health status
  • diet
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30
Q

What are the symptoms of Congenital muscular dystrophy?

A

Abnormal muscle hypotonia and weakness in a newborn child with dystrophic muscle biopsy

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31
Q

Which is the most common sub-type of Congenital muscular dystrophy?

A

Most common sub-type is MDC1A, in which the mutation is in extracellular lamin alpha2.

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32
Q

Treatment in Dementia?

A

4 drugs are used: 1) cholinesterase inhibitors: donepezil, rivastigme, galantamine

  • Stabilize cognitive performance and daily functions
    2) Glutamate antagonist: memantine
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33
Q

How is dementia diagnosed?

A

In general: history of the patient, neuropsychological tests, assesments of symptoms

  • vascular dementia: no established way of diagnostics
  • dementia with lewy bodies: visual hallucinations, parkinsonism, progressive cognitive failure
  • frontotemporal dementia: change in behavior, implusitivity, aggressivity
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34
Q

Is dementia genetic or inherited?

A

Majority is not inherited

In FTD causative genes: C9orf72, CRN, MAPTR and risk genes: CTCS, postiive family history

-Early stage alzheimer (5%) PSEN 1, PSEN 2, APP

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35
Q

Treatment for Huntington’s disease?

A
  • Gene therapy, stem cell therapy
  • invariably fatal disease
  • Blueberries (improve survival in cell expressing mHTT)
  • Block crosslinking or reducing aggregates, or reduction of HTT aggregates
  • restore impaired signalling

For chorea: dopamine receptor antagonists, dopamine depleting

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36
Q

How is Myotonic dystrophies characterised?

A

Myotonic dystrophy is an RNA repeat toxicity mediated disease.

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37
Q

How many types of Myotonic dystrophies there is?

A

Two. Type 1 and Type 2. Type on can present at any age and type 2 is present mostly between ages 20 and 40.

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38
Q

What are causing Metabolic myopathies?

A

Caused by biochemical defect in metabolism of carbohydrate, lipid and adenine nucleotides. Inherited disorders.

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39
Q

What therapy is used in metabolic myopathies?

A

subjective improvement on ketogenic diet which is low carbohydrate

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40
Q

What are are genetic myopahties (=Muscular diseases)?

A
  • Congential myopathy
  • Muscular dystrophy
  • Myotonic dystrophy
  • Myotonia congenita
  • Metabolic myopathy
  • Periodic paralysis
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41
Q

Is inflammatory genetic myopathy (=muscle disease)?

A

No, it is acquired muscle diseases. Different dystrophies are genetic diseases.

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42
Q

What are the common symptoms of muscle diseases?

A

Weakness
Atrophy
Fatigue
Pain and/or cramps

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43
Q

Diagnostic studies of muscle diseases?

A 
Electromyography
Muscle magnetic resonance imaging (MRI)
Spiroergometry
Autoantibodies
Genetic testing
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44
Q

Risk factors for HD and who may become affected?

A
  • individuals more than 36 repeats in HD gene
  • individuals having the risk to inheriting the expanded CAG nucleotide
  • de novo mutation( mutaatio munasolussa tai siittiössä)
  • parent having it
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45
Q

Is multiple scelorosis inherited?

A

No, but there is a genetic risk, at least 110 risk genes which affect on leukocytes like HLA-DR15, DQ6

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46
Q

What is causing the dystrophies?

A

Typically dystrophies are caused by mutations that impair the structural support of sarcolemma. These mutations usually happens in dystrophin or its co-operators.

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47
Q

How are dystrophies classified?

A

Dystrophies are classified based on their underlying gene defect

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48
Q

In where the mutation is in Duchenne muscular dystrophy?

A

Mutation is in X-lined DMD gene that is encoding dystrophin

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49
Q

What is the onset ot Duchenne muscular dystrophy (DMD)?

A

first symptoms around 2-6 years

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50
Q

Does DMD (deuchenne muscular dystrophy) lead to death?

A

Yes. Heart and respiratory failure usually lead to death by early 20s, but survival age 30-40 is possible.

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51
Q

What are special cases of DMD?

A
  • Becker muscular dystrophy

- Woman carriers (usually DMD occurs only in men)

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52
Q

What happens if the mutations of DMD disturb the reading frame of DMD protein?

A

Mutations that disrupt the reading frame of DMD result in complete loss of dystrophin

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53
Q

What is the goal in therapy related to DMD?

A

Goal is to restore dystrophin expression at sarcolemma

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54
Q

What are early symptoms of limb gridle muscular dystrophy (LGMD)?

A

Difficulty rising stairs, difficulty elevating arms. These symptoms develop slowly

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55
Q

How is the LGMD herited?

A

Either autosomal dominant or autosomal recessive

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56
Q

What is the onset of Congenital muscular dystrophy?

A

Newborns

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57
Q

What are the symptoms of Congenital muscular dystrophy?

A

Abnormal muscle hypotonia and weakness in a newborn child with dystrophic muscle biopsy

58
Q

Which is the most common sub-type of Congenital muscular dystrophy?

A

Most common sub-type is MDC1A, in which the mutation is in extracellular lamin alpha2.

59
Q

What is the treatment for Congenital muscular dystrophy?

A

Treatment is supportive

60
Q

What are symptoms for FSHD (Facioscapulohumeral muscular dystrophy)?

A

alking gradually deteriorated, difficulty walking stairs, tripping on threshold and carpets, “strange” position when walking, foot drop

61
Q

Is the family history often negative in FSHD?

A

Yes

62
Q

Where is the mutation in FSHD2?

A

mutation in SMCHD1

63
Q

Where is the mutation in FSHD1?

A

mutation in D4Z4 contraction

64
Q

What are two myopathies related to distal myopathy?

A
  • Welander distal myopathy and UDD distal myopahty.

- In Welander the mutation is in TIA1 gene and in UDD the mutation is in TNN gene

65
Q

What is causing Metabolic myopathies?

A

Caused by biochemical defect in metabolism of carbohydrate, lipid and adenine nucleotides. Inherited disorders.

66
Q

What therapy is used in metabolic myopathies=

A

subjective improvement on ketogenic diet which is low carbohydrate

67
Q

What are the molecural genetics behind the metabolic myopathies?

A

variant in PFKM gene

68
Q

What are the four types of inflammatory myopathy?

A
  • Dermatomyositis (DM)
  • Polymyositis (PM)
  • Immune-mediated necrotizing myopathy (NM)
  • Inclusion body myositis (IBM)
69
Q

What is causing inflammatory neuropathy and is it genetic?

A

It is caused by or associated with immune activation. NOT GENETIC MUSCLE DISEASE!

70
Q

What are the symptoms of inflammatory neuropathy?

A

Slowly progressive proximal and distal weakness of quadriceps, wrist and finger flexors and ankle dorsi reflectors

71
Q

How many genes there is that have mutations that can affect to the arise of the muscular dystrophies?

A

Muscular dystrophies can arise from mutations in more than 40 different genes

72
Q

Due to what DM2 (type 2 myotonic dystrophies) happens?

A

Due to mutations in CNBP gene

73
Q

What are symptoms to DM2 (type 2 myotonic dystrophies)?

A

Most often starts with stiffness and pain in thigh muscles in one or both legs (stiffness in fingers -> difficulty to open jars)

74
Q

Course of Alzheimer:

A

AB accumulation or failure in misfolding AB-> AB oligomers -> deposition (gradual)->intermediates(välittää) diffuse amyloid plaques ->accumulatiom of AB aggregates and fibrils form amyloid plaques-> phosphatase and kinase (->neurofibrillary tangles) and inflammatory response (->oxidative stress)—–>neuronal and synapse dysfunction-> cognitive dysfunction

75
Q

Risk factors for PD?

A

Age
Family
Gender
Protective environmental factors: coffee, cigarettes
Suspected environmental risk factors- no consistent evidence: well water use, rural dwelling (maalaisasuminen tai joku), mining (kaivostyö)
Altered gut microbiome
exposure to antibiotics

76
Q

Different types of Parkisonism:

A

Parkinson’s disease

Secondary parkinsonism: Vascular, infectious, drugs/toxins, metabolic, tumor/trauma, normal pressure hydrocephalus

Hereditary: PARK gene/loci, spinocerebellar ataxias, huntigtons disease, wilsons disease, neuronal brain iron accumulation disorders

Atypical parkinsonism:

  • Corricobasal degeneration
  • Multiple system atrophy
  • Dementia with Lewy bodies
77
Q

Is PD genetic?

A

-10-15% has family history
PARK, PINK1, PRKN (autosomal recessive)
LRRK2, SNCA (autosomal dominant)
-lot of gene-environment interactions

78
Q

Basic mechanisms of Parkinson’s disease?

A
  • alpha-synuclein protein folding disruptions-> forms Lewy bodies
  • Can be seen in substantia nigra as depigmentation and paleness, which is caused by neuronal loss, gliosis
  • Degeneration of substantia nigra-> causes motor symptoms
  • A premotor phase for several years (REM sleep problems, constipation(ummetus), olfactory problems, depression..)
  • Motor symptoms emerge after
    • 50% of nigral cell loss
    • 80%of striatal DA loss
  • Gastrointestil dysfunctions
also changes in:
cerebral cortex
multiple brainstem & basal forebrain nuclei
hypothalamus
spinal cord
Peripheral ANS
enteric NS
79
Q

Treatment of Parkinson’s disease?

A
  • Levadopa therapy
  • MAO-B inhibitors
  • COMT inhibitors
  • Dopamine antagonists
  • Surgical therapy
80
Q

Risk factors for MS?

A

Genetic factors

  • antigen presentation
  • T-lymphocyte apoptosis
  • T-lymphocyte proliferation (increase)
  • Cell adhesion (yhteenkasvu)
  • Lymphocyte development

Environmental factors

  • Epstein-Barr virus (EBV) other viruses?
  • lack of UV-light
  • lack of D vitamin
  • smoking
  • organic solvents
  • teenage obesity

Early development

  • Mont of birth effect
  • T-cell development
  • Lack of vitamin D
81
Q

Basic mechanism of MS?

A
  • multiple autoimmune attack in brain optic nerve and spinal cord oligodenrocytes
  • dysfunction of leukocytes –> growth of autoimmune clones
  • genes encoding for (HLA-DR2)
  • plaques in sensory pathways

COURSE:
relapsing 90%
progressive 10% ->microglial play a role

82
Q

Treatment of MS?

A

-Lowering of body temperature

-For urinary incontinence:
Sphincter muscle training
Training of “bladder and soul”
Anticholinergic drugs inhibit bladder wall muscle contraction
Botox in special cases injected to bladder wall
Catheterisation, if residual urine volume < 1 dl

-For Neuropathic pain:
Epilepsy- or depression drugs that have pain refusing affect

-Disease modifying drug:
Immunomodulation
Migration inhibition
cytotoxity

83
Q

Risk factors for cronification of migraine:

A 
obesity
low educations
female
diabetes
arthritis
allodynia
high fequency og migraine attacks (>10 headache days per month)
too much pain medications, especially opioids
84
Q

Primary causes of migraine?

Pathway of the pain?

A

1) hyperexcitable brain
- CSD from visual cortex
- cortical spreading depression leads to aura: first intense cortical neuron activity->followed bt neuronal suppression-> headache

2) The dysmodulated brain, activation starts in dorsal pons

  • Trigeminal-vascular activation:
    1. Meninges->Neurogenic inflammation and vessel dilation
    2. Trigeminal ganglion, Activation of pain signalling
    3. Second-order brainstem neurons
    4. Headache pain in the sensory cortex
85
Q

Diagnosis of migraine?

A
  1. By symptoms
  2. Red flags
    - systematic symptoms (fever, weight lost..) and secondary risk factors (HIV, cancer)
    - neurologic symptoms or abnormal signs
    • older (usually appears in young adults): new onset and progressive headage
    • previous headache history: first headache or different (change in attack frequency etc)
86
Q

Hereditary of migraine?

A

runs in families in 90% of patients

87
Q

Causes for headaches?

A
  • primary headaches: migraine, tension-type, cluster headache
  • secondary headaches: tumor, meningitis, giant cell arteritis
88
Q

course and symptoms of migraine:

A
  1. Predromal symtoms: graving for food, tiredness, irritability
  2. Neurological aura symptoms: visual, sensory, speech disturbance, hemiparetic(toispuoleinen heikous), vertigo
  3. Vascular headache: Moderate to severe, unilateral, pulsing, made worse by physical activation, associated with nausea, vomiting, sensitivity to light and sounds
  4. Postdromal symptoms: Hangover, tiredness, burst of energy
89
Q

Treatment of migraine?

A

-avoidance of triggering factors (alcohol, lack of sleep, stress etc)
-acuate medications (NSAIDs, tritans, anti-emetics etc)
-preventive medications(antihypertensives, tricyclic antidepressants)
-non-pharmaceutical treatment (acupuncture)
-CGRP antibodies
Calcitonin gene-related peptide (CGRP)
involves multiple processes such as:
combinations of medicine most efficient: sumatriptan + metoclopramide

90
Q

Risk factors for depression?

A
  • family history of mental illness
    -chronic physical or mental disorders
    a stressfull change in life patterns
    psychological factors
    -low socioeconomic status
    -female gender
    -insomnia, sleep disorders
91
Q

Basic mechanisms of depression, hypothesis (not known)?

A
  • Lack of serotonin
  • too little neurogenesis
  • too little plasticity
  • sleep rhythm disturbances
  • neural circuits are affected in depression
92
Q

Heredity of SZ?

A
  • strong genetic background
  • Heterogenous, multiple genetic risk factors, partially shared with other psychiatric disorders
  • all together over 200 disease associated loci
  • High heritability but no genetic variation is deterministic- the role of environment
93
Q

How is SZ diagnosed?

A

-2 or more symptoms:
hallucinations, delusions, disorganized speech and/or behavior, lack of speech, diminished emotional expression

  • medical history
  • ongoing for 6 months

-exclusion of other disorders by MRI, CT and bloodtests

94
Q

Risk factors in SZ?

A
  • Genetic
  • Season of birth
  • Pregnancy and birth complications
  • Maternal infection during pregnancy
  • Pro-inflammatory cytokines in the maternal serum during pregnancy
  • urban birth and upbringing
  • migration
  • cannabis use
  • stressful life events and early childhood trauma
95
Q

What the patients may also complain in PD (clinical manifestations)?

A
  • Small hand writing
  • Masked face
  • Muscle cramps
  • Reduced blinking
  • impairments in manual tasks

etc

96
Q

What treatment is used in Parkinson’s disease?

A
  • Surgical therapy

- Drug therapy (levodopa, Da antagonist, MAO-B inhibitor, COMT inhibitor) and even drug combinations

97
Q

What is Parkinsonism?

A

A clinical syndrome characterized by slowness and poverty of the movement, stiffness. There is multiple different causing reasons: like other degenerative disorders, drug-induces, toxic, metabolic etc.

98
Q

What are four different classes of Parkinsonism?

A

Parkinson’s disease, Hereditary Parkinsonism, Secondary Parkinsonism, Atypical Parkinsonism

99
Q

Risks for SMAJ?

A
  • Patients with chareot-marie-tooth neuropathy

- Male (64%)

100
Q

What happens in DBS?

A

Doctor implants tiny electrodes in the part of the brain that regulates mood

101
Q

What happens in SMAJ?

A
  • Benign (hyvälaatuinen) motor neuron disease

- Loss of motor neurons in spinal cord

102
Q

Genes in SMA?

A

mutation in SMN1 gene in chromosome s9

103
Q

What are four different classes of Parkinsonism?

A

Parkinson’s disease, Hereditary Parkinsonism, Secondary Parkinsonism, Atypical parkinsonism

104
Q

What is the main cause of motor symptoms in PD?

A

Degeneration of substantia nigra

105
Q

Mechanism of huntington’s disease?

A

Repeats of CAG over 36 times-> 36 or more glutamines->accumulation in dorsal striatum-> neuronal cell death because of excitotoxity caused by excessinve signaling->high Ca2+

DNA polymerase adds extra CAGs-> more repetitions->more unstable disease

Decreased GABA and acetylcholine, Increased dopamine

More repeats cause symtoms in earlier life

106
Q

Symptoms of HD?

A

-progressive CNS involvement->movement (chorea and athetosis “snake-like”movememnts), cognitive (dementia, personality changes, depression), mood

107
Q

What happens in DBS?

A

Doctor implants tiny electrodes in the part of the brain that regulates mood

108
Q

What happens in TMS that is used as an treatment method in depression?

A
  • Stimulates nerve cells in affected brain areas

- improve symptoms of depression

109
Q

What different types of epilepsy there are?

A

Simple partial

  • on the other side of the brain
  • conscious
  • strange sensations
  • jerking movements
  • often remembers
  • patient knows something is happening

Complex partial

  • Both hemispheres, front part of the brain
  • impaired consciousness
  • OR impaired awareness and responsiveness
  • may not remember

Generalized seisures

  • Both hemisphere
  • unconscious
  • Tonic (falls back), atonic(falls forward), clonic (attack on the ground), tonic-clonic, myoclonic (short muscle twitches), absence (lose and regain conciousness)
110
Q

symptoms following seizure?

A
  • postictal confusion
  • Todd’s paralysis (paresis): in arms or legs, last average 15 min, subsites complitely 2 days, temporary or severe suppression of seizure-affected area
111
Q

Diagnosis of epilepsy?

A
  • Brain imaging MRI,CT->look for abnormalities e.g. tumors
  • EEG->detect electrical signals in brain
  • Because epilepsy varies, diagnosis requires tests and examination of clinical history
112
Q

Treatment of epilepsy?

A
  • Daily medication: anticonulstants, wide variety
  • Epilepsy surgery
  • Nerve stimulation-> stimulate vagus nerve-> influences neurotransmitter release
  • Ketonic diet->force body to burn fat and use kerone bodies as energy instead of glucose
113
Q

Stroke mechanisms and how can it be devided?

A

Brain does not get enough oxygen!

  • Hemorrhagic stroke->artery breaks, intracerebral and on the cortex, pia mater
  • Ischemic stroke-> blocked artery, more common, damage depends on location, time
  • > if the blood clot dissolves-> transient ischemic attack (TIA) “mini stroke”
114
Q

Signs and symptoms of stroke?

A 
FAST=
F: face, other side droops
A: arm weakness (+legs)
S: speech, slurred
T: time-> call immediately

CT scan and treatment follows

115
Q

Treatment of stroke?

A

First few hours after stroke: tissue can’t be saved afterwards

  1. TPA “The clot buster medicine” dissolves clot
  2. Thrombectomy- minimally invasive: for larger clots

Afterwards: recovery slow

  • Recovery may works with speech therapy, physical therapies, occupational therapy
  • Depression common after stroke, support important

Preventing another stroke and maximize quality of life

116
Q

Risk factors for stroke?

A
  1. Hypertension-high blood pressure
  2. Smoking
  3. Diabetes-causes high blood sugar
  4. high cholesterol

-can be reduced with lifestyle changes and medication
Medication: daily aspirin, blood thinners

117
Q

What are main genes in early onset AD?

A

Gene effects in three genes: Presenilin 1,Presenilin 2, Amyloid precursor protein

118
Q

What are the symptoms of anxiety disorder?

A

There are many, but in example:

  • feeling nervous, tense, fearful
  • chest pain
  • panic attacks
  • rapid heart rate
  • fatigue
  • shaking
  • restlessness
119
Q

How can anxiety disorder be diagnosed?

A

By physical examination (is anxiety linked to some medication / medicational condition), psychological examination, by blood/urine test to exclude other causes

120
Q

Who are at risk of developing anxiety disorder?

A

Women are more in risk than me, adults under age 35, people with chronic diseases (e.g. cancer, diabetes)

121
Q

What are risk factors of anxiety disorder?

A

Chronic psychosocial stress especially in early life, negative life events, dysfunction in CRF regulation

122
Q

How can be anxiety disorder treated?

A

By psychotherapy (cognitive-behavioral therapy, exposure therapy), by medicines (SSRis, 5-HT antagonist). If any of those did not work, also TMS and DBS can be used.

123
Q

Is anxiety inherited?

A

Heritability of anxiety disorder is 30-60% which is quite large. However, even more affecting than genes is environment.

124
Q

Genetics of anxiety disorder?

A

Various susceptibility genes found: e.g. 5-HTT and BNDF. However, the contribute of these genes is only 1-2% -> environment has bigger affect

125
Q

Basic mechanism of anxiety?

A

Scrambled brain connections, chemical imbalances, dysbalanced processes in relevant neuro circuitries like GABA-ergic system.

126
Q

Is anxiety genetics heterogeneous?

A

yes.

127
Q

What causes seizures in epilepsy?

A

too many brain cells becomes exiting simultaneously -> neurons synchronously active. Too much excitation or too few inhibition (GABA receptors dysfunction)

128
Q

When epilepsy is consider to be resolved?

A

Epilepsy is considered to be resolved for individuals who had an age-dependent epilepsy syndrome but are now past the applicable age or those who have remained seizure-free for the last 10 years, with no seizure medicines for the 5 years

129
Q

Treatment for AD?

A
  • no cure
  • cholinesteraze inbitors (Donepezil, Galantomine)
  • NDMA antagonists (Memantine)
130
Q

What gene mutations cause autosomal dominant self-limited epilepsy?

A

Mutations in KCNQ2 and KCNQ3.

131
Q

What are KNCQ2 and KCNQ3?

A

Channels that form homo- and heterotetramers (proteins) that are responsible for M-current (a slow inactivating K+ current). This M-current constraint repetitive neuronal firing.

132
Q

How are NMDA receptors linked to epilepsy?

A

There are seven NMDA receptor subunits each encoded by their respective gene (GRIN1 etc). Mutations in epilepsy patients have identified in those NMDA receptor genes GRIN1, GRIN2A, 2B,2D.

133
Q

What genes are related to focal epilepsies?

A

CHRNA4, LGl1, DEPDC, GRIN2A, GRIN2B, GRIN2D

134
Q

In which two categories can de novo mutations in epilepsy be divided?

A

Missense mutations and protein truncation mutations

135
Q

What are the known “Epilepsy genes”?

A
  • Ligand gated ion channel genes
  • Voltage gated ion channel genes
    Other epilepsy genes (cover 73% of these three gene cateory)
136
Q

In which three categories can epilepsy seizures be divided?

A
  • Focal
  • Generalized
  • Unknown
137
Q

What are risk factors for epilepsy?

A
  • Age
  • Family history
  • Head injury
  • Brain infection (like meningitis)
  • Seizures in childhood
  • Dementia
138
Q

Diagnosis for epilepsy?

A 
by EEG (looking for abnormalities), brain scan, blood test.
-Epilepsy can be diagnosed only if the person has have at least one seizure
139
Q

Six types of generalized seizures?

A
  • Tonic
  • Clonic
  • Tonic & clonic
  • Myoclonic
  • Atonic
  • Absence seizures
140
Q

two categories of focal seizures?

A
  • Focal seizures without loss of consciousness

- Focal seizures with impaired awareness

141
Q

What is SNOOP in migraine?

A

SNOOP is used in the diagnose of migraine. It means:

  • Systemic of symptoms or secondary risk factors (e.g. HIV)
  • Onset (sudden or?)
  • Older
  • Previous headache history

Basic mechanisms of nervous system diseases (12 decks)

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