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Brain Disease Flashcards

1
Q

General neurological assessment of patients will include…

A 
Cognitive function
Gait 
State of consciousness 
Mental state, attitude insight 
Co-ordination/fine movements 
Cranial nerves 
Motor system (wasting, tremor, power, tone, reflexes) 
Sensory system (touch, pain, vibration, 2 point discrimination)
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2
Q

General psychiatric assessment will include…

A

Appearance and general behaviour
Mood and affect
Speech, disorders of thought (stream, form, content)
Insight
Abnormal beliefs and perceptions
Cognitive state (concentration, confusion, memory)

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3
Q

Parkinson’s symptoms

A 
Decrease in spontaneous movements 
Gait difficulty 
Postural instability 
Rigidity 
Tremor
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4
Q

Pathology of Parkinson’s

A

Degeneration of pigmented neurons in the substantia nigra of the brain
Decreased dopamine availability

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5
Q

Incidence of Parkinson’s

A

1-2%
Frequency increases exponentially after 60 years
Higher incidence in developed countries

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6
Q

Are men or women more affected by Parkinson’s

A

Both equally affected

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7
Q

Where is the most effective site for deep brain stimulation in Parkinson’s patients?

A

Subthalamic nucleus (STN)

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8
Q

What frequency of DBS alleviates Parkinson’s symptoms?

A

> 60 Hz

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9
Q

What frequency of DBS exacerbates Parkinson’s symptoms?

A

< 30 Hz

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10
Q

What is the hypothesis behind DBS for Parkinson’s patients?

A

Stimulation prevents low frequency rhythm generation and desynchronises the extrastriatal basal ganglia and cortex

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11
Q

Does Parkinson’s have a monogenetic basis?

A

<10% monozygotic twins show concordant expression of PD

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12
Q

Why do the substantia nigra dopamine neurons die in Parkinson’s disease?

A

Most cases are idiopathic
Aberrant proteostasis
Environmental factors which disrupt mitochondrial function e.g. pesticides

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13
Q

What are the genetic forms of Parkinson’s disease?

A

Associated with mutations in the a-synuclein, Parkin, PINK1, DJ-1, LRRK2, ATP13A2, PLA2G6
Identical mutations in family members can be associated with different onsets and severities

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14
Q

21st century treatments for Parkinson’s disease

A

Protection
Regeneration
Stimulation

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15
Q

Protection against Parkinson’s disease

A

Voltage-gated Ca2+ channel blockers, glial derived neurotrophic factor (Amgen)

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16
Q

Regeneration in Parkinson’s disease

A 
Transplantation 
Stem cells (induced, embryonic)
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17
Q

Stimulation in Parkinson’s disease

A

Smart stimulators

Optogenetics

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18
Q

Who first described Parkinson’s disease?

A

Dr. James Parkinson

1817

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19
Q

Who first described Huntington’s disease?

A

George Huntington

1872

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20
Q

Symptoms of Huntington’s disease

A

Progressive hyper/dyskinesias followed by akinesia and dystonia and dementia/psychoses

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21
Q

Incidence of Huntington’s disease

A

Rare

0.04-0.1%

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22
Q

Pathology of Huntington’s disease

A

Autosomal dominant hereditary disease

Abnormal number of CAG

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23
Q

Animal models suggest that ____ _____ is the initial trigger in Huntington’s disease

A

Cortical dysfunction

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24
Q

Role of mutant huntingtin

A
  • Important for synaptic vesicle dynamics and transmitter release
  • Pathological changes due to widespread not specific expression of mutant huntingtin
  • Pathology due to aberrant circuit activity
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25
Treatments for Huntington's disease
- Memantine - Tetrabenazine - Deep brain stimulation - RNA interference - Stem cell transplantation
26
Positive symptoms of schizophrenia
- Delusions - Hallucinations - Disordered thought and speech
27
Negative symptoms of schizophrenia
- Flat affect - Alogia (inability to speak) - Anhedonia (inability to feel pleasure) - Asociality (lack of motivation to engage in social activity) - Avolition (decrease in the motivation to initiate and perform self-directed purposeful activities)
28
Pathology of schizophrenia
Increased levels of dopamine in the mesolimbic pathway
29
Incidence of schizophrenia
0.6% of population worldwide
30
When does schizophrenia start?
Can start at any age, peak onset early 20s
31
Causes of schizophrenia
- Genetic - Environment - Development - Social factors - Drug abuse - Dopamine hypothesis - Reduced NMDAR function
32
Treatment of schizophrenia
- Antipsychotics (+ve symptoms) | - Intense psychotherapy
33
Symptoms of depression
- Lowered mood - Anhedonia (lack of pleasure in activities) - Avolition (decrease in the motivation to initiate and perform self-directed purposeful activities) - Altered appetite - Hyposomnia/hypersomnia - Worthlessness and guilt - Reduced ability to concentrate - Recurrent thoughts of death - Reduced life span - 3-7%
34
Pathology of depression
- Reduced hippocampal volume - Vascular lesions - Reduced BDNF (brain-derived neurotrophic factor)
35
Incidence of depression
- 3% Japan - 18% USA - 10% average - Women 2x more than men
36
Causes of depression
- Genetic 5-HT transporter abnormalities - Monoamine hypothesis - Psychological (self, others, future) - Social (poverty, stress, abuse)
37
Treatment of depression
- Light therapy - Psychotherapy - Tricyclic antidepressants - SSRIs - Exercise - ECT
38
Types of clot
- Ischaemic | - Haemorrhagic
39
Ischaemic stroke
- Embolus (wandering clot) - Thrombus (local clot) - Systemic hypoperfusion - Venous thrombosis
40
Haemorrhagic stroke
Entry of blood into CNS via rupture of a blood vessel/sinus or an aneurysm
41
Classification of haematoma affecting the brain
- Epidural - Subdural - Subarachnoid - Intracerebral
42
Epidural haematoma
Traumatic damage to a meningeal artery or dural venous sinus (blow to the head)
43
Subdural haematoma
Is caused by rapid movement of head causing tearing of the cerebral vein as it enters a dural venous sinus
44
Subarachnoid haematoma
Is caused by damage to a cerebral artery or vein and subsequent bleeding into the subarachnoid space
45
Intracerebral haematoma
Cause by damage of a blood vessel within the brain
46
Incidence of stroke
- 10% of deaths worldwide | - 95% occur > 45 years
47
Top 3 causes of death worldwide
1. Heart disease 2. Stroke 3. Cancer
48
Cause of stroke
Ischaemic cascade - ATP production reduced - Ion pumps fail - Glutamate levels rise - NMDA receptors activated - Ca enters neurons - ROS/free radicals produced - Cell death - Inflammatory response may further exacerbate damage
49
Risk factors of stroke
- High blood pressure - High cholesterol - Diet - Physical inactivity - Drugs of abuse (alcohol, cigarettes, cocaine, amphetamine)
50
Preventative treatments for stroke
- Preventative - Anticoagulants - Carotid angioplasty/endarterectomy - Diet/lifestyle
51
Acute ischaemic treatments for stroke
- Thrombolysis - tissue plasminogen activators (within 3 hours) - Thrombectomy - Angioplasty/stenting
52
Acute haemorrhagic treatments for stroke
Surgery
53
Chronic post stroke treatments
- Control of hypertension - Aspirin - Physical and occupational therapy
54
Types of epilepsy
- Partial/focal | - Generalised
55
Incidence of epilepsy
- 0.5-1.0% | - 5% will experience a non febrile seizure
56
Childhood absence epilepsy
- 4 - 12 years of age - Absence seizures (10-30 second episodes of unresponsivity, sometimes with eye rolling, lip smacking, hand shaking) several hundred per day
57
Characteristic wave in childhood absence epilepsy
3 Hz spike-wave discharge
58
Mutation in childhood absence epilepsy
Mutation in low threshold voltage-dependent Ca channels
59
How is childhood absence epilepsy resolved?
Without pathology in puberty
60
Temporal lobe epilepsy
- Late childhood and adolescence - Most common type in adults - Complex partial seizures often with aura - May develop into secondary generalised tonic-clonic/grand mal seizures
61
Where is the epileptogenic focus in temporal lobe epilepsy?
In hippocampus and/or amygdala and/or parahippocampal gyrus (recurrent excitatory circuits)
62
Causes of epilepsy
- 2/3 idiopathic - Reflex seizures precipitated by a trigger (light) - Genetic - mutations in Na+ channels - Cerebrovascular disease - Tumours - Alcohol/drugs - Trauma/hypoxia - Infection - Metabolic disorder - Development disorder - Degenerative disorder - Pathological synaptic plasticity (producing an imbalance in excitation and inhibition in the nervous system)
63
Acute treatments for epilepsy
- Generalised or complex partial seizures - recovery position - Simple partial seizures - reassurance, maintain safe environment - BZs
64
Chronic treatments for epilepsy
- Pharmacological - ethosuximide (blocks/modulates Ca and Na channels) carbamazepine (modulates Na+ channels potentiates GABA receptors) - Surgical - removal of tumour, AVM (Brain Arteriovenous Malformations) or epileptogenic tissue (temporal lobe, hippocampus) - Electrical - vagal, deep brain stimulation - Avoidance of seizure triggers
65
Symptoms of Alzheimer's disease
- Short-term memory loss - Progressive apathy, confusion, irritability, mood swings, long term memory loss, withdrawal, loss of control of bodily functions - Death within 7 years of diagnosis
66
Pathology of Alzheimer's disease
- Profound loss of neurons - Plaques (amyloid B) - Neurofibrillary tangles (hyperphosphorylated tau)
67
Incidence of Alzheimer's disease
1.5 - 2.0%
68
Causes of Alzheimer's disease
- Age, 10% over 65, 50% >84 - Genetics predominately for early onset (ApoE4 gene variant) - Trauma - High blood pressure - Hypercholesteremia - Environmental factors
69
Treatment of Alzheimer's disease
- Acetyl cholinesterase inhibitors - NMDA receptor antagonists (memantine) - NSAIDs and caffeine - Intellectual stimulation - Diet - Exercise

BMS Neuroscience (23 decks)

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