Final Flashcards
1
Q
Neurological Disorders
A
Any disorder of the body nervous system
2
Q
Stroke
A
Loss of brain function due to lack of blood and O2
3
Q
Stroke Risk Factors
A
Hypertention (high blood pressure)- 35-50% risk
Atrial Fibrillation - 5% risk
High Cholesterol
Diabetes mellitus
4
Q
Stoke Symptoms
A
Hemiplegia- paralysis one side of body
Hemiparesis- weakness one side of body
Hemineglect- lack or awareness on one side of thebody
Dysphagia- Difficulty swallowing
Dysarthia- Diffucult speaking, facial weakness
Aphasia- Diffuculty speaking and understanding speech, damage to language centers
5
Q
Two arteries to brain
A
Common Carodid Artery
Vertebral Artery
6
Q
Types of Stroke
A
Ischemic- blood clot
Hemorrhagic- Blood leaks into brain tissue
7
Q
Infarct
A
Occurs after 3 hours of damage, permanent damage due to lack of nutrients, o2 to brain
8
Q
Penumbra
A
At risk healthy brain tissue near the Infarct.
9
Q
Stroke Exitotoxicity
A
- Lack of blood
- Depolarization
- Too many action potentials
- opening of NMDA and glutamate receptors, Influx of CA and Zn
- Ca and Zn induce apoptosis.
10
Q
Stroke Treatments
A
- Get rid of blood clot
- Reduce # of action potentials
- block glutamate receptors, Ca, Zn channels
- Rehabilitation
- Physical therapy, occupational therapy, speech therapy, psychological treatment
- IPSC stem cell therapy- replace dead neurons with new stem cells from skin
11
Q
Head Injuries
A
TBI- Traumatic brain injuries- Most common from falls then car accidents
12
Q
Concussions
A
Head injury from the blow to the head with out penetration.
13
Q
Coup/ Countercoup
A
Coup is where the brain hits the skull and the countercoup is the rebounce hit to skull
14
Q
Concussion Damage
A
bent, or torn brain tissue at the junction between the axon and soma
15
Q
Brain Hematoma
A
Epidural- between bone and dura mater
Subdural- between dura mater and arachnoid
Intercerebral- within the brain hemoraggic
16
Q
Dementia Pugilistica
A
Features of dementia cuased by repeated damage to brain
17
Q
Dementia Pugilistica is the Accumulation of …
A
Tau Protien, start at frontal cortex and then to amygdala and hippocampus and respective symptoms
18
Q
Dementia Pugilisitca
A
Loss of neurons, scarring of brain tissue, plaques, neurofibrillary tangles
19
Q
Types of Tumors
A
Gliomas- of glial cells (50.4%)
Meningoimas - of meninges (20.8%)
Pituitary adenomas - of pituitary gland (15%)
Nerve sheath tumors - of myelin around nerves (8%)
20
Q
Tumor Treatments
A
Surgery to remove
Radiotherapy to kill
No chemotherapy since it can’t cross the BBB
21
Q
Epilepsy
A
Long-term epileptic seizures
22
Q
Seizures
A
Abnormal excessive and synchronous neuronal activity
23
Q
Types of seizures
A
Partial simple- Clear area of origin no loss of consciousness
Partial Complex- loss of consciousness
Generalized- no clear area, large area effected by seizure
-Grand Mal- violent convulsions
-petit mal- brief period of unconsciousness
24
Q
Lack of inhibition in Epileptic seizures
A
- GABA neuron loss
- Miswiring
- Lose of GABA receptor
- Disinhibition
25
Seizure treamtent
1. Gaba agonist
| 2. Surgery if due to structural issues (corpus callosumectomy)
26
Neurocysticercosis
Pork Tapeworm infection of brain
27
Neurocysticercosis symptoms
seizures
Increased intercranial pressure and hydrocephalus (CSF blocked)
Back pain if cysts are in spinal cord.
28
Treatment of parasite infections
Anti-seizure medicine
Anti-worm medicine
Surgery to remove cysts
Prevention: vaccine pigs, cook meat
29
Encephalitis
Acute inflammation of brain due to bacteria, virus, fungi
30
Encephalitis Symptoms
Headache, fever, confusion, drowsiness, fatigue,
Severe symptoms: seizures, tremors, memory issues
31
Encephalitis causes
```
Rabies virus
Herpes simplex
Poliovirus
measles virus
West Nile Virus
```
32
Primary Encephalitis
Virus directly invades the CNS (ex west nile)
33
Secondary encephalitis
virus invades first other parts of the body then brain
34
Meningitis
Inflammation of meninges and spinal cord, caused by bacteria in CSF (Milky spinal tap)
35
Brain inflamation and swelling restricts blood flow leading to...
Damage and symptoms
36
Meningitis symptoms
Headache, stiff neck, fever, confusion, vomiting, inability to tolerate light or loud noises.
37
Transmissible Spongiform Encephalophaties (TSE)
Digs holes in brain, (spongiform) Ex. Prion Disease
38
Prion disease
Microscopic holes are seen in brain
39
Prion Symptoms
memory changes, personality changes,movement problems
40
Prions cause normal proteins of prion proteins to be misfolded
These cause apoptosis of neurons as misfolded prion proteins enter and burst neurons
41
Types of prion disease
1. Mad Cow disease.
| 2. Creutzfeldt-Jakob Disease (CJD) - human nerological disorder that is incurable and fatal
42
CJD death and pathway to symptoms
Misfolded proteins enter neuron and then replicate then burst neuron to be released into brain.
5% genetic cause, acquired by eating cows with Mad cow dissease or scrappies with prion disease
43
Multiple sclerosis (MS)
autoimmune condition and inflammatory disease in which the myelin are damaged.
44
MS symptoms
vision problems, stiff muscles, numbness in arms and legs, bladder control loss, mental physical fatigue, mood changes,
45
Secondary progressive MS (SPMS)
Follows RRMS, continuous increase of symptoms, no remission
46
Relapsing-remitting MS (RRMS)
Most common, includes relapes folowed by remission but a gradual inclease in MS symptoms as each occur
47
Primary progressive MS (PPMS)
Steady worsening of neurological functioning without distinct relapses
48
Progressive- relapsing MS(PRMS)
Steady worsening with occasional attacks, relapses
49
MS affects...
only the white matter, immune system attacks the myelin, leads to inflammation and lesions in brain
50
Cause of MS
No clear cause, combination of genetic, and environmental,
51
Ataxias
Problems moving
52
Dementias
Problems thinking
53
Alzheimer's
Most common form of dementia, no cure
54
Symptoms of Alzheimers
difficulty remembering, confusion, aggression, mood swings, language troubles, long term memory loss, withdraw
55
Alzhermers Cause
Plaques of beta amyloid in grey matter of brain
Neurofibrillary tangles due to phosphorylation of Tua protein
Inflamation
56
Familial form of AD
Dominant inheritance with onset before 65
Mutation of APP, Presenilin 1, presenilin 2 genes.
57
Sporadic AD
Most forms of AD, caused by combination of genetic and environmental conditions.
58
Genetic risk factor of AD
inheritance of e4 allele of the APOE gene
59
Environmental risks AD
Head trauma, high cholesterol, high blood pressure
60
3 hypothesis of AD
1. AB plaques hypothesis: Plaques form first then disease cascades
2. Cholinergic hypothesis of AD (inflammation first)- Low Acetylcholine= inflammation
3. Tau hypothesis: Tau protein clumps up, leads to microtubules falling apart and forming tangles.
61
AD prevention and treatment
Boost acetocholine levels, reduce glutamate exitotoxicity.
62
Parkinsons
Degenerative disorder of dopamine-generating cells in substantia Nigra
63
Parkinsons Lack of Dopamine
Lack of activation of Basal Gangila to inhibit motor signals leading to loss of muscle control (tremors)
64
Parkinsons Treatment
Increase dopamine levels, MAO-B inhibitors to prevent degradation of dopamine.
Levodopa helps replace dopamine
65
Huntington
Genetic disorder that affects muscle coordination and cognitive and psychiatric decline.
66
Cause of Huntington
Genetic dominant mutation of Huntington (HTT) gene.
40+ repeat of CAG
36-39 may or may not be HTT effected
<35 will not be effected
67
HTT gene interaction
Effects Transcription, cell signalling, Caspase Activity- protein involved in apoptosis.
68
Huntington disease effects
Striatum degeneration, hippo campus, substantia nigra
69
Huntington patients show...
general atrophy of cortical tissue, enlarged ventricles.
70
Tetrabenazine
dopamine antagonist- reduce Chorea (sporatic movements)
71
Gene silencing
reduce HTT effect
72
Schizophrenia
Mental disorder characterized by a breakdown of thinking and emotional responses.
No sex bias, but men have a earlier onset (18-25)
73
Schizophrenia Positive, Negative, Cognitive deficits
Positive- symptoms that should not be present (hallucinations, delusions)
Negative- symptoms that are a lack of character (reduced speech, lack of emotions, social withdrawal)
Cognitive deficits- Memory issues, attention issues, decision making issues
74
Schizophrenia causes
Genetic and environmental causes (old damaged sperm, Cannabis comsumption before 18, stress, Prenatal mother has an infection, Hypoxia)
Genetic - Disc1.... lots of genes
75
Brain strucutre in schizophrenia
1. Enlarged Ventricles- lose of neurons in those areas.
2. Hippocampal cells are disorganized leading to cognitive deficits. More disoriented the more severe the disorder.
3. Lower frontal lobe activity- lower executive functioning.
4. decreased acivity in lateralization of brain
5. Loss of grey matter in adolescent brain
76
Biochemistry of schizophrenia
Dopamine hypothesis: Too much dopamine leads to schizophrenia. Dopamine antagonists seem to help schizophrenia but only the positive symptoms not the negative symptoms
Glutamate hypothesis: Reduced glutamate activity leads to schizophrenia. Trying to develop drugs to boost Glutamate signaling.
77
Atypical antipsychotics
improve the negative symptoms of Schz (Clozapine - serotonin agonist)
78
Major Depressive disorder
Depression most of the day with lost of interest in normal activites DSM-V: at least 2 weeks everyday
Lifetime prevalence of 20-25%
79
MDD causes
genetic: 5-HTT (Serotonin transporteer)- short allele= less transporter= reduced reuptake= depression? but Prozac reduces reuptake and seems to help depression
80
Clock gene and SCN in depression
Circadian rhythm disturbance leads to depression
81
Envioment for MDD
Very high Cortisol can lead to depression, stress
82
MDD structural abnormalities
Decreased hippocampus volume, and orbitofrontal cortex, decreased activity of Anterior cingualte cortex - role in rational fucntions and reward anticipation, decision-making, increased amygdala- emotional and emotional memory.
Decreased left hemisphere and increased rt activity= more negative less happy
83
Biochem of Depression
HPA axis is overactive, and there is irregular circadian rhythms of cortisol secretion. The negative feedback of HPA axis may be inhibited.
84
Monoamine in MDD
Lack of Serotonin- anxious irritable
Lack of Noradrenaline- loss of energy and interest
Lack of Dopamine- lack of happiness and enjoyment in life
85
SSRI
Help increase levels of serotonin in MDD patients
86
ECT for MDD
Electroconculsive shock therapy
Electrodes are used to control eletical currents in patientes head, causes brief seizures and seems to be effective for severely depressed.
87
Bipolar disorder
Mood disorder characterized by unusual shifts in mood, energy, activity, and drive
88
Mania
excessive energy excitement, illusions of grandiosity
89
Bipolar causes
High genetic relationship, high concordance rate with twins, some similar behaviors and genes with schizophrenia,
Enviromental causes: prenatal mother has depression, psychosis and especially bipolar disorder.
Messed up sleep-wake cycle can induce bipolar disorder and shifts between depression and mania
90
Bipolar brain structure
Reduced hippocampal volume and elevated basal ganglia activity increased amygdala volume and activation. Overall increased activity in the BP brain
91
Bipolar biochemestry
Too much Norepiniphrine= mania
| Too little serotonin= depression
92
Anxiety disorders
Difficulty regulating and controlling anxiety, with symptoms around excessive and irrational fear and dread.
93
OCD
- Intrusive thoughts that produce uneasiness, fear, worry
| - Repetitive behavior to reduce associated anxiety
94
OCD causes
Gene and enviromental (head trauma, seizures etc)
Brain strucutrue- under activation of area responsible for stopping habitual behaviors (lateral orbitofrontal cortex), abnormal connetions between basal ganglia and frontal cortex
95
OCD biochem
low serotonin levels
96
PTSD
Recurrent thoughts of traumas, that impair daily functioning.
97
PTSD brain structure
Shrinkage of hippocampus, and porr negative feedback of HPA axis= more coritsol in system.
Overactivation of the amygdala
98
PTSD treatments
Psychotherapies (exposure thereapy)
Antidepressants
GABA agonists
99
Autism Spectrum Disorder
Neurodevelopmental disorder,
Difficulties in social interactions, verbal and nonverbal communcaiton and repetitive behavior
Sex biased, males more likely than girls.
100
Autism Genetics
Strong genetic contribution to autisms
101
Autism enviroment
Prenatal Sodium Valporate to control mother's bipolar disorder- led to decreased migration of neurons of babies, big scandal
102
Autism brian strucutre
Small head at birth then large increase during first few years of life. Lack of synaptic pruning, too much connections in brain. Smaller corpus callosum in autism
103
Biochemistry of Autism
Too high glumate to GABA ratio. Too much excitation= social disorganizaiton.
Reduced activity in the serotonin transporer= low serotonin levels in the brain but high levels in the blood
104
Autism Treatments
Early intervention therepy to teach social and cognitive language skills
SSRI
Antipsychotics to reduce aggression and act on dopamine system
105
ADHD
problems with attention, hyperactivity, impulsivity. These must begin by age 6-12
106
ADHD causes
genetic and enviromental (over 50% is genetic) the rest is prenatal smoking/alcohol/lead, premature and low birth rate
107
ADHD Brian strucutre
Less total grey matter, and inpairments in prefrontal cortex- inattention and impusivity and impaiments in basal ganglia leads to hyperactivity.
108
ADHD biochem
reduced level of dopamine, treat with ritalin- dopamine agonist (reuptake inhibitor)
109
ADHD treatments
Diatary changes-food resptrictions, reduce inflamation foods
Psychotherepay- earlier the better, EEG feedback and behavior thereapies.
Medication- ritalin
