Module 5.1 Neurology Flashcards
1
Q
What is the Biogenic Amine Theory?
A
Biogenic amine theory: Depression is due to a deficiency of neurotransmitters in the brain, primarily norepinephrine, serotonin and dopamine. Particularly a decrease in receptor binding with serotonin.
2
Q
What is the Neurotransmitter receptor hypothesis?
A
- Neurotransmitter receptor hypothesis: deficiency of monamine neurotransmitters, especially norepinephrine, dopamine, and /or serotonin. Depletion of these neurotransmitters is thought to result in up-regulation of some post-synaptic receptors.
- The neurotransmitter receptor hypothesis refers to decreased levels of monoamine neurotransmitters at the neuronal synapses. Antidepressants increase neuronal synaptic levels of these monamine neurotransmitters. You must have sufficient neurotransmitters to attach to receptors in order for ‘communication’ to exist between the neurons. Most of the neurotransmitters will be released from the receptors after their ‘communication’ between the neurons- this is when the neurotransmitters ‘recharge’ themselves and get ready to re-attach to a receptor. So if you have more receptors than neurotransmitters, your neurotransmitters don’t have time to re-charge- so they don’t function properly.
3
Q
How does stress contribute to depression?
A
- HPA Dysregulation
- Hypothalamic-Pituitary-Adrenal (HPA) System plays an essential role in an individuals ability to cope with stress.
- Uncontrollable stress activate the immune system. A potential consequence of prolonged cytokine induced activation is disregulation in feedback and feedforward control mechanisms of the HPA system, leading to chronic elevation of cortisol
- Excessive glucocorticoid (cortisol) secretion is found in about 30-70% of people with major depression.
- Elevated cortisol levels throughout the evening and early morning is associated with depressed people.
- Not all antidepressants regulate the HPA system dysregulation
4
Q
What is Alzheimer Disease?
A
Alzheimer Disease is the leading cause of dementia and one of the most common cause of severe cognitive dysfunction in older adults.
- Nonhereditary, or sporadic, late onset AD is the most common form
- Early onset familial AD (FAD) is autosomal dominant and has been linked to gene defects.
- The pathology for both is identical
5
Q
What are pathologic alterations of the brain seen in Alzheimer Disease?
A
- formation of neuritic plaques containing a core of amyloid beta protein.
- formation of neurofibrillary tangles
- degeneration of basal forebrain cholinergic neurons with loss of acetylcholine
- loss of ACh and other neurotransmitters contribute to the loss of memory, attention, and other cognitive functions..
6
Q
How is an increased production or deposit of amblyoid B protein in the brain thought to cause Alzheimer Disease?
A
Failure to process and clear amyloid precursor protein resultts in the accumulation of toxic fragments of amyloid beta protein that leads to the production of diffuse neuritic plaques, disruption of nerve impulse transmission and death of neurons
Amyloid also is deposited in cerebral arteries causing amyloid angiopathy and disturbance in blood flow
7
Q
How are neurofibrillary tangles formed?
A
- The tau protein, a microtublule binding protein, in neurons detaches and forms an insoluble fillament called neurofibrillary tangle, with contribute to neuronal death
- The loss of neurons results in brain atrophy with decreases in weight and volume
8
Q
What is Parkinsons Disease?
A
- PD is a complex motor disorder accompanied by systemic nonmotor and neurologic symptoms. The main disease feature is degeneration of the basal ganglia involving the dopaminergic (dopamine secreting) nigrostriatal pathway. This causes hypokinesia, tremor, and muscular rigidity
9
Q
What is the hallmark pathologic features of Parkinson Disease?
A
progressive death of dopaminergic pigmented neurons in the substantia niagra (SN) pars compacta with dopaminergic deficiency in the putamen portion of the striatum
10
Q
What is the pathology of motor movement in Parkinson Disease
A
- Degeneration of dopaminergic nigrostriatal pathway to tha basal ganglia results in underactivity of the direct motor pathway (normaly facilitates movement). This results in inhibition of of the motor cortex manifested with bradikinesia and rigidity.
- Degeneration of dopaminergic neurons in the nigrostriatal system of the substantia nigra leads to dopamine depletion. The substantia nigra is part of the basal ganglia of the brain, an area that receives input from many areas of the brain including the cerebral cortex and helps to coordinate motor activity. In this area 2 opposing pathways (direct and indirect) maintain a balance that results in coordinated motor movements. Loss of dopamine leads to inhibition of cortically initiated movements (controlled by the direct pathway) and excitation of receptors in the indirect pathway that produce involuntary tremors.
11
Q
What is a thrombotic stroke (cerebral thrombosis)?
A
- Thrombotic stroke arise from arterial occlusions caused by thrombi formed in the arteries supplying the brain or in the intracranial vessels.
- Attributed to atherosclerosis and inflammatory disease process that damage arterial walls
12
Q
What causes an embolic stroke?
A
- Fragments that break from a thrombus formed outside the brain or in the heart, aorta, or common carotid artery. Other sources of embolism include fat, air, tumor, bacterial clumps, and foreign bodies.
- Usually emboli originate in the heart and are a result of diseased cardiac valves or arrhythmias
- Hypercoagulable states
- Conditions like polycythemia, dehydration, sickle crisis, etc. may cause a blood clot to form and obstruct a vessel
13
Q
What is a Subarachnoid Hemorrhage
A
- Blood escapes from a defective or injured vasculature into the subarachnoid space where normally there is only CSF.
- Bleeding may originate from a ruptured artery, leaking arteriovenous malformation, or blood dyscrasia.
14
Q
What is a Intracerebral hemorrhage stroke?
A
- A blood vessel leaks or ruptures directly into brain tissue
- The cause may be hypertension, arteriovenous malformation, or blood dyscrasia
15
Q
What is multiple sclerosis?
A
- MS is a chronic inflammatory disease involving degeneration of CNS myelin, scarring or formation of plaque, and loss of axons.
- An autoimmune disease that produces diffuse demyelization with plaque formation, usually in white matter but can extend to grey matter. The result is abnormal nerve conduction.
16
Q
What triggers inflammation in Multiple Sclerosis?
A
- Some viral particles resemble myelin antigens, “molecular mimicry”. This causes the immune system to attack both viral particles and myelin.
- Autoreactive T and B cells recognize myelin autoantigens and trigger inflammation in the CNS, leading to the loss of myelin sheaths and nerve conductivity and subsequently to the death of neurons
18
Q
Generally, what are the two types of seizures?
A
-
Generalized Seizures:
- involve neurons bilaterally
- often do not have local (focal onset)
- usually originate from a subcortical or deeper brain focus.
- consciousness always is impaired or lost
-
Focal Seizures (partial seizures):
- involve neurons only unilaterally
- often have a local onset
- originate from discrete areas usually associated with structural abnormalities localized to the cortical brain tissue, thereby having a superficial focus.
- Consciousness may be mantained as long as seizure activity is limited to one hemisphere in simple partial seizures.
19
Q
What is a simple partial seizure?
A
- Simple Partial
- An aura may precede the seizure
- Consciousness is maintained
- Motor symptoms may include abnormal movement or an arm, leg or both
- There may be abnormal sensory symptoms (sounds, smells, body sensations)
- Autonomic symptoms may include a change in heart and/or respiratory rate
- There may be psychic symptoms (fear, deja vu)
- Duration is seconds to minutes
20
Q
What is a complex partial seizure?
A
- Complex Partial
- Consciousness is impaired but not lost
- The eyes may be open, but the person may not be able to respond to questions or commands (or give inappropriate responses)
- There may be automatisms (e.g. lip smacking, picking at clothing)
- There may be bizarre behaviors (e.g. running, removal of clothing, screaming)
- Speech may be jumbled or repetitive
- There may be posturing or jerking movements
- There may be progression to a secondary tonic-clonic seizure
- Duration is seconds to minutes
Post ictal confusion and amnesia are common
21
Q
Describe a generalized Absence sizure
A
- Absence
- Brief (5-10 second) loss of consciousness
- May many times each day
- Blank stare or eye blinking
- No postictal period. Normal activity is resumed immediately following the seizure
22
Q
Describe a myoclonic seizure
A
- Myoclonic
- There are short abrupt muscle contractions or the arms, legs or torso. These may be strong enough to cause a fall or cause a person to drop objects.
- Duration: seconds
23
Q
Describe a clonic seizure
A
- Clonic
- Muscle contraction and relaxation with jerking movements
- Both sides of the body are involved
- Duration: may last several minutes
24
Q
Describe a tonic seizure
A
- Tonic
- Sudden stiffening movements of the arms, legs and torso. Both sides of the body are involved
- Commonly occur during sleep
- Duration: usually less than 20 seconds
25
Q
Describe a tonic-clonic seizure
A
- Tonic-Clonic
- Loss of consciousness
- Contraction of respiratory muscles forces exhalation and may produce a cry
- Stiff body
- Tonic phase with symmetrical extension or extremities, eyes rolled up or to the side, tongue may be bitten
- Clonic phase with jerking after which the person becomes flaccid.
- Urine and fecal incontinence
- Post ictal phase characterized by exhaustion.
26
Q
Describe a atonic seizure
A
- Atonic
- Abrupt loss of muscle tone causing the person to fall
- Duration: seconds
- Postictal confusion
27
Q
Describe anxiety disorders
A
- most prevalent psychiatric disorders
- fears that are abnormal, intense, irrational and severe enough to interfere with the lives of affected persons.
- Young adults are most often affected.
- Women are affected more often than men.
- Somatic symptoms are often present.
28
Q
Describe a generalized anxiety disorder
A
- Generalized Anxiety Disorder: uncontrollable chronic worry that is unrealistic and excessive, persisting for at least 6 months. Somatic symptoms may include tachycardia, palpitations, tremor, gastrointestinal upset
29
Q
Describe a panic disorder
A
- Panic Disorder:
- discrete periods of intense fear or terror, accompanied by somatic or cognitive symptoms.
- Attacks are sudden, peak rapidly and last for less than 30 minutes. They are accompanied by a sense of impending doom and an urge to escape.
- Patients begin to avoid situations that precipitate attacks. Often leads to agoraphobia.
- Dysregulation of the brain GABA-benzodiazepine receptor system may contribute to the development of panic attacks.
30
Q
What is social phobia?
A
- Social Phobia: extreme, persistent fear of social or performance situations. This can impair one’s occupational or academic accomplishments.
31
Q
Describe Obsessive Compulsive Disorder
A
- Obsessive-Compulsive Disorder:
- recurrent obsessions that cause marked anxiety and/or compulsions to neutralize the anxiety.
- Thoughts and images occur repeatedly and precipitate compulsive ritualistic behavior.
- Obsessions may involve dirt, germs, toxins, orderliness, religion, etc.
- Affected individuals are often aware that their behavior is abnormal, but are unable to stop it.
32
Q
Describe Post-Traumatic Stress Disorder
A
- Post-Traumatic Stress Disorder: occurs after involvement or witnessing of an event that involved actual or threatened death or serious injury to self or others that is repeatedly re-experienced. This may include combat, natural disasters, assaults, etc. Symptoms of avoidance numbing, and difficulty sleeping are present for more than 4 weeks.
33
Q
What is phenylketonuria (PKU)?
A
- PKU is an autosommal recessive inborn error of metabolism characterized by mutations of the phenylaline hydroxylase (PAH) gene.
- Congenital error of metabolism where there is an inability of the body to convert the essential amino acid phenylalanine to tyrosine. Tyrosine is needed to synthesize protein, melanin, thyroxine, and the catecholamines in the brain and adrenal medulla. Failure to convert the phenylanine to tyrosine results in increased levels of phenylalanine causing CNS damage (mental retardation, hyperactivity, seizures).
34
Q
What causes Attention Deficit Hyperactivity Disorder
A
- Pathology:
- excessive frontal lobe activity.
- genetic predisposition.
- The problem is not caused by excessive sugar or additives in the diet
35
Q
What is a migraine headache?
A
- An episodic neurologic disorder whose marker is headache lasting 4-72 hours.
- characterized by recurrent throbbing headaches, varying in intensity, frequency and duration, but sharing common characteristics. These are accompanied by nausea, photophobia and phonophobia
36
Q
What is the Neurovascular hypothesis behind migraines?
A
- Neurovascular hypothesis:
- A trigger alters a specific area of the brainstem called the locus ceruleus and triggers release of serotonin into the trigeminal vascular tree. Not all patients are able to identify a trigger. Those commonly identified include lack of sleep, stress, hormonal changes, physical exertion, weather changes or certain foods (most commonly wine caffeine, monosodium glutamate, nitrates, and artificial sweeteners). It is controversial whether factors thought to be triggers, e.g. chocolate, are actually cravings that are part of the prodromal phase.
- A sterile perivascular inflammatory process occurs
- Pain sensors in the ophthalmic branch of the trigeminal nerve become active and release neuropeptides that cause dilation of blood vessels. This produces even more nerve irritation.
- The inflammatory response and distended blood vessels stimulate the trigeminal nerve; producing pain long after the trigger is gone
37
Q
What causes migraines during menstrual periods?
A
Menstrual migraines are thought to be triggered by changes in estrogen levels. Estrogen levels rise after ovulation. This may sensitize the cranial vessels to changes in hormone levels. Falling levels of estrogen during the premenstrual period may trigger the onset of migraine
38
Q
What is Myasthenia Gravis?
A
Myasthenia Gravis is a chronic autoimmune disease mediated by acetylcholine receptor (AchR) antibodies that act at the neuromuscular junction
- Onset of symptoms is gradual over a period of 5-7 years.
- The most common initial symptoms are ocular disturbances, e.g. ptosis and/or diplopia. This may spread to facial and oropharyngeal muscles, causing weak smile, and difficulties with chewing, swallowing, or speaking.
39
Q
What causesMyasthenia Gravis?
A
- MG results from a defect in nerve impulse tranmission at the neuromuscular junction. The main defect is T-cell dependent formation of autoantibodies (IgG) against receptors at the Ach binding site on the postsynaptic membrane
- Antibodies attack and damage acetylcholine receptors at neuromuscular junctions. This results in a loss of receptors and decreased impulse transmission to muscles. The end result is weakness.
- cause of this autosensitization is unknown
40
Q
Describe the neurotransmitters that could be involved in the different types of anxiety disorders (i.e. panic).
A
- Dysregulation of the brain GABA-benzodiazepine receptor system may contribute to the development of panic attacks.
- Gamma-amino butyric acid (GABA)
- Inhibition (counteracts neuronal excitation).
- Increased levels in depression
- Altered in panic disorder related to a reduction in the benzodiazepine (BZ) receptor binding. BZ plays a role in GABA producing a neuronal inhibitory effect.
41
Q
Explain the process of neurotransmitter transmission between 2 neurons
A
