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BMS Neuroscience > Brain Disease > Flashcards

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
Q

Treatments for Huntington’s disease

A
  • Memantine
  • Tetrabenazine
  • Deep brain stimulation
  • RNA interference
  • Stem cell transplantation
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26
Q

Positive symptoms of schizophrenia

A
  • Delusions
  • Hallucinations
  • Disordered thought and speech
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27
Q

Negative symptoms of schizophrenia

A
  • 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)
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28
Q

Pathology of schizophrenia

A

Increased levels of dopamine in the mesolimbic pathway

29
Q

Incidence of schizophrenia

A

0.6% of population worldwide

30
Q

When does schizophrenia start?

A

Can start at any age, peak onset early 20s

31
Q

Causes of schizophrenia

A
  • Genetic
  • Environment
  • Development
  • Social factors
  • Drug abuse
  • Dopamine hypothesis
  • Reduced NMDAR function
32
Q

Treatment of schizophrenia

A
  • Antipsychotics (+ve symptoms)

- Intense psychotherapy

33
Q

Symptoms of depression

A
  • 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
Q

Pathology of depression

A
  • Reduced hippocampal volume
  • Vascular lesions
  • Reduced BDNF (brain-derived neurotrophic factor)
35
Q

Incidence of depression

A
  • 3% Japan
  • 18% USA
  • 10% average
  • Women 2x more than men
36
Q

Causes of depression

A
  • Genetic 5-HT transporter abnormalities
  • Monoamine hypothesis
  • Psychological (self, others, future)
  • Social (poverty, stress, abuse)
37
Q

Treatment of depression

A
  • Light therapy
  • Psychotherapy
  • Tricyclic antidepressants
  • SSRIs
  • Exercise
  • ECT
38
Q

Types of clot

A
  • Ischaemic

- Haemorrhagic

39
Q

Ischaemic stroke

A
  • Embolus (wandering clot)
  • Thrombus (local clot)
  • Systemic hypoperfusion
  • Venous thrombosis
40
Q

Haemorrhagic stroke

A

Entry of blood into CNS via rupture of a blood vessel/sinus or an aneurysm

41
Q

Classification of haematoma affecting the brain

A
  • Epidural
  • Subdural
  • Subarachnoid
  • Intracerebral
42
Q

Epidural haematoma

A

Traumatic damage to a meningeal artery or dural venous sinus (blow to the head)

43
Q

Subdural haematoma

A

Is caused by rapid movement of head causing tearing of the cerebral vein as it enters a dural venous sinus

44
Q

Subarachnoid haematoma

A

Is caused by damage to a cerebral artery or vein and subsequent bleeding into the subarachnoid space

45
Q

Intracerebral haematoma

A

Cause by damage of a blood vessel within the brain

46
Q

Incidence of stroke

A
  • 10% of deaths worldwide

- 95% occur > 45 years

47
Q

Top 3 causes of death worldwide

A
  1. Heart disease
  2. Stroke
  3. Cancer
48
Q

Cause of stroke

A

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
Q

Risk factors of stroke

A
  • High blood pressure
  • High cholesterol
  • Diet
  • Physical inactivity
  • Drugs of abuse (alcohol, cigarettes, cocaine, amphetamine)
50
Q

Preventative treatments for stroke

A
  • Preventative
  • Anticoagulants
  • Carotid angioplasty/endarterectomy
  • Diet/lifestyle
51
Q

Acute ischaemic treatments for stroke

A
  • Thrombolysis - tissue plasminogen activators (within 3 hours)
  • Thrombectomy
  • Angioplasty/stenting
52
Q

Acute haemorrhagic treatments for stroke

A

Surgery

53
Q

Chronic post stroke treatments

A
  • Control of hypertension
  • Aspirin
  • Physical and occupational therapy
54
Q

Types of epilepsy

A
  • Partial/focal

- Generalised

55
Q

Incidence of epilepsy

A
  • 0.5-1.0%

- 5% will experience a non febrile seizure

56
Q

Childhood absence epilepsy

A
  • 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
Q

Characteristic wave in childhood absence epilepsy

A

3 Hz spike-wave discharge

58
Q

Mutation in childhood absence epilepsy

A

Mutation in low threshold voltage-dependent Ca channels

59
Q

How is childhood absence epilepsy resolved?

A

Without pathology in puberty

60
Q

Temporal lobe epilepsy

A
  • 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
Q

Where is the epileptogenic focus in temporal lobe epilepsy?

A

In hippocampus and/or amygdala and/or parahippocampal gyrus (recurrent excitatory circuits)

62
Q

Causes of epilepsy

A
  • 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
Q

Acute treatments for epilepsy

A
  • Generalised or complex partial seizures - recovery position
  • Simple partial seizures - reassurance, maintain safe environment
  • BZs
64
Q

Chronic treatments for epilepsy

A
  • 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
Q

Symptoms of Alzheimer’s disease

A
  • 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
Q

Pathology of Alzheimer’s disease

A
  • Profound loss of neurons
  • Plaques (amyloid B)
  • Neurofibrillary tangles (hyperphosphorylated tau)
67
Q

Incidence of Alzheimer’s disease

A

1.5 - 2.0%

68
Q

Causes of Alzheimer’s disease

A
  • Age, 10% over 65, 50% >84
  • Genetics predominately for early onset (ApoE4 gene variant)
  • Trauma
  • High blood pressure
  • Hypercholesteremia
  • Environmental factors
69
Q

Treatment of Alzheimer’s disease

A
  • Acetyl cholinesterase inhibitors
  • NMDA receptor antagonists (memantine)
  • NSAIDs and caffeine
  • Intellectual stimulation
  • Diet
  • Exercise

BMS Neuroscience (23 decks)

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