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Brain and Behavior > Exam 4 Deck 1 > Flashcards

Exam 4 Deck 1 Flashcards

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1
Q

What are primary headache syndromes?

A

Physiological disruption

Migraine
Tension type

Cluster

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2
Q

What are secondary headache syndromes?

A

Pathology + physiology

Neoplasm

Infection

Aneurysm

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3
Q

What is the most common type of headache?

A

Tension headache

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4
Q

What is the most common type of headache that physicians see?

A

Migraines

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5
Q

What defines a migraine without aura?

A

At least 5 attacks

Headache lasts 4-72 hours

Two of: unilateral, pulsatile, moderate/severe pain, aggravation or avoidance of physical activity

One of: N/V, photophobia and phonophobia

Not attributable to somethign else

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6
Q

What defines a migraine with aura?

A

At least two of:

Aura with fully reversible visual, sensory, or dysphasic speech symptoms

Homonymous visual or unilateral sensory symptoms; 1 aura symptom developing over 5 minutes, or different symptoms in succession over 5 minutes

Headaches fulfill criterea for migraine without aura

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7
Q

How does cerebral blood flow correlate with headache?

A

Prodrome - nothing

Aura - nothing

Headaceh - increased flow

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8
Q

How do you determine whether the origin of a headache is opthalmic?

A

All ocular causes of headache are associated with changes in the external apperance of the eye

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9
Q

How do the timing and topography of cerebral blood flow, aura, and headache relate to each other during migraine attacks?

A

Pain begins during hypoperfusion phase

Hyperperfusion may outlast pain

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10
Q

What is cortical spreading depression?

A

Devleopment of waveform in brain that causes period of activation followed by refractory period of depression

Crawls at 3mm/minute from brainstem, up to occiput, and then forward through brain

I.e. activation = aura; depression = blindness

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11
Q

Describe threshold of transcranial magnetic stimulation of a patient with migraines compared to normal.

A

Migraines - lower thereshold (brain is ‘excitable’)

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12
Q

What brain structures get activated at the onset of migraines?

A

Brainstem centers - periaqueductal grey turns on during migraine attack

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13
Q

What structures is primarily involved in migraines that can explain symptoms?

A

Meninges!

Cortical spreading depression causes release of vasodilatory mediators in the brain that cause meninges to expand/be inflamed

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14
Q

What is the cheiro oral phenomenon?

A

Numbing/tingling of cheek and hand (which then spreads)

Almost pathognomonic for migraines

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15
Q

If a patient walks in with headache symptoms and a tingling/numbing of the mouth and a hand, that progressively spreads up arm, what are you thinking?

A

Migraine

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16
Q

What is the funciton of glial cells, and what about their normal physiology is important to migraines?

A

They redistribute K, Mg, and excitatory amino acids

Lowest numbers in primary occipital cortex (i.e. if glia aren’t working well, the occipital lobe will take a hit)

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17
Q

What is the role of astrocytes in migraines?

A

Astrocyte calcium waves could mediate propagated cortical phenomena of migraine via release of neuroactive and vasoactive messengers

Astrocyte waves can explain cortical activity changes in the absence of cortical spreading depression

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18
Q

What is a tension-type headache?

A

Bilateral, band-like pressing headache

Not aggravated by activity

Little or no nausea, photophobia, or phonophobia

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19
Q

What are the diagnostic criteria for tension-type headache?

A

Essentially: not a migraine

Bilateral, steady non-pulsatile pain, not affected by movement,

Not associated with N/V, nor photophobia nor phonophobia

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20
Q

Can migraines present with neck pain?

A

yes

Migraines are often misdiagnosed because of neck pain leading to the diagnosis of tension headache

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21
Q

What is the physiology of neck pain that can be seen in migraines?

A

It is a referred pain phenomenon

Trigeminal nucleus caudalis extends to dorsal horn C2, C3, C4 => causes neck pain and posterior head pain.

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22
Q

What is the trigeminal autonomic reflex?

A

Irritation of trigeminal nerve causes activaiton of parasympathetic nucleus which causes lacrimation, rhinorrhea, nasal congestion

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23
Q

What is the tearing/sniffling/congestion reaction to cold/spicy/etc called?

A

Trigeminal autonomic reflex

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24
Q

What are some symptoms of children with migraines?

A

Benign paroxysmal vertigo of childhood

Alternating hemiplegia

Cyclic vomiting

Recurring abdominal pain

Benign torticollis

Acute confusional migraine

Car sickness

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25
Q

What is sinus headache?

A

NOT actually a thing.

Commonly diagnosed as headache secondary to sinusitis in the US - leads to overprescription of antibiotics

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26
Q

What are more serious complications of migraines?

A

Progression in severity

Migrainous stroke

Persistent aura without infarction

Epilepsy

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27
Q

What neurological issues does migraine put you at an elevated risk for?

A

Stroke

Epilepsy

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28
Q

What are you likely to see if you order an MRI for a migraine patient?

A

White matter changes that may be misdiagnosed as MS plaques, vasculitis, etc.

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29
Q

Generally speaking, what is the timeframe of primary headache syndromes?

A

Months to years

Shorter is likely to be a secondary headache

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30
Q

Which structures in the head are pain sensitive?

A

Meninges

Neural Structures (Trigeminal, Glossopharyngeal, Vagus CNs)

Scalp + Superficial structures

Vasculature

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31
Q

What are red flags that a headache is not a primary headache syndrome?

A

• A new or different headache

– ≤5 years old

– ≥50 years old

  • Abrupt onset
  • Cancer, HIV, pregnancy
  • Abnormal physical exam
  • Neuro symptoms ≥ one hour
  • Headache onset

– With seizure or syncope – With exertion, sex, or

Valsalva

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32
Q

How do headaches due to brain tumors present?

A

Similar to tension headaches in most patients

Can be migraine like

“Classical” brain tumor headache is only 8%

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33
Q

What type of headache do patients with brain abscesses get?

A

Same as brain tumor

Fever in 1/2 of cases

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34
Q

Patient with frontal headache which increase with straining and are awekening out of sleep. Also papiledema, and dysmenorrhea. What type of headache?

A

Idiopathic intracranial hypertension

Pseudotumor cerebri

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35
Q

What are characteristics of headaches of idiopathic intracranial hypertension?

A

brain tumor headache

Visual complaints (diploplia, TVOs, photopsias)

Cranial bruits, noises in head, pulsatile tinnitus

N/V

radiculopathies

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36
Q

What do you treat idiopathic intracranial hypertension with?

A

Try to correct predisposing factors (weight loss, diuresis, shunting)

Try to preserve vision - optic nerve sheath fenestration

Symptoms

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37
Q

What is a hypnic headache syndrome?

A

Rare disorder in older people (40-84 y/o)

Bilateral throbbing headache

Recurring 1-3 times nightly with no other associated symptoms

Treat with lithium, caffeine, flunarizine

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38
Q

What types of headaches are seen with patients who had strokes?

A

Abrupt or gradual

Severity not associated with size of infarct

Headache can be multifocal or migratory - pain can move down arms, etc)

Not migraine in older patients (would have had a history)

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39
Q

What must you consider in a patient with “complicated” migraine presentation who is older?

A

Not only migraine (but may be less likely due to age)

Consider tumors, strokes, sensory seizures, etc.

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40
Q

How do sub-arachnoid hemmorage present as?

A

Abrupt onset of severe headache (reaches full intensity instantly - or close)

(Aneurysm burst)

Seizures and diploplia can be seen

Perform non-contrast CT, LP

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41
Q

What is thunderclap headache?

A

Headache seen in survivors of Berry aneurysm

Can be caused by aneurysmal or nonaneurysmal subarachnoid hemmorrage

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42
Q

What distinguishes a thunderclap headache from a subarachnoid hemmorrhage?

A

Seizures adn diploplia seen in SAH

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43
Q

What is a cluster headache?

A

Intense, boring (knife-like pain, very severe), unilateral pain

Quicker onset (over span of minutes)

Eyes tear and nose runs - autonomic involvement

Horner’s Syndrome (ptosis and miosis)

Episodic - bouts of headache that last 1-4 months. Follow circadian pattern within and between cycles

Chronic - may evolve from episodic form or be chronic from onset. Absence of circadian patterns

Headaches with manic symptoms - almost opposite of migraine

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44
Q

What is temporomandibular dysfunction?

A

Pain that can be around the ear while chewing

Can go away quickly, but can persist too

Click may be heard over ear while jaw opening.

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45
Q

What type of headache can present with giant cell arteritis (temporal arteritis)?

A

Generalized, throbbing, temporal pain

Claudication - worsens with exertion

Polymyalgia rheumatica in 50% (aches and pains, maybe fever)

Visual scintillations

CRP or ESR abnormalities indicate biopsy

TREAT WITH CORTICOSTEROIDS

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46
Q

What type of headaches can be seen with angina?

A

Jaw, tip of nose, brow, bregma, occiput, palate, …. (anywhere really)

Extremities, shoulder pain

Rarely below umbilicus

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47
Q

What type of headache do you see with sexual activity?

A

Explosive, throbbing, occipital or frontal

Lasts for hours

Confusional state or symptoms of ischemia

(occur with valsalva too)

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48
Q

What symptoms can you see withs pontaneous carotid artery dissection?

A

Seen in young and middle age

Risk factors include trauma, arteriopathies, family history, respiratory infection

Headaches, neck pain, horner’s syndrome

Cerebral ischemia

Tx: anticoagulation

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49
Q

If a patient presents with unilateral throbbing headache with pain of the face, neck, worse with movement, Horner’s Syndrome, and a recent URI; what do you suspect?

A

Spontaneous carotid artery dissection

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50
Q

What can cause low-pressure headache?

A

Meningeal diverticula

Dural root sleeve tears

Excessive coughs

Erosion of dura from adjacent lesions

Head trauma

overshunting/carbonic anhydrase inhibitors

Lumbar puncture (esp. in thin females)

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51
Q

What is a common issue that can develop in thin female patients who have lumbar punctures?

A

Low-pressure headacehs

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52
Q

How do you treat low-pressure headaches?

A

IV Na caffeine benzoate

Epidural blood patch (if post-LP)

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53
Q

What is beta-2-transferrin?

A

Indicator of CSF

If seen in rhinorrhea, indicative of CSF leak

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54
Q

What do you suspect if you identify beta-2-transferrin in rhinorrhea?

A

CSF leak

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55
Q

What is POTS?

A

Postural orthostatic tachychardia syndrome

Seen in young post pubertal females

See orthostatic and non-orthostatic headache

Fatigue, decreased concentration, exercise intolerance, syncope

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56
Q

How do you treat POTS?

A

Hydration and salts

Elastic stockings

Beta blockers, fludrocortisone, minodrine, indomethacin

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57
Q

72 year old male, developed sharp pains in his right cheek and lip. These increased with light touch and he was nearly unable to shave or eat. His neurological examination was entirely normal. What do you suspect?

A

Trigeminal Neuralgia

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58
Q

What is trigeminal neuralgia??

A

Brief paroxysms of electric-like, lancinating pains (stabbing)

Usually affects V2 and V3

Stimulation of trigger points induces attacks

Suggest structural disease - demyelinated nerve-root area

Seen more in older patients. In younger patients think neurodegenerative disease

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59
Q

How does trigeminal neuralgia occur in older patients?

A

Superior Cerebellar Artery rubs against trigeminal nerve root and causes demyelination - origin of pain

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60
Q

How does trigeminal neuralgia occurs in younger patients?

A

Demyelinating process of trigeminal nerve

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61
Q

What is primary stabbing headache?

A

New onset, sharp, shooting pain in temple and behind eye

Not triggered by cutaneous stimuli

Preceded by days of euphoria

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62
Q

What sequence of events occurs during excitotoxicity?

A

Injury (ischemia, trauma, etc) leads to a decreased ATP state in the neuron.

This causes increased Na and Ca levels, depolarizing membrane potential.

Glutamate is increased extracellularly, exciting neighboring neurons.

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63
Q

What is chromatolysis?

A

Apoptosis of neurons

Shown here surrounded by healthy neurons with intact Nissl bodies

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64
Q

What is neurapraxia?

A

Focal demyelination of a neuron

Leads to a loss in conduction velocity of the axon - neuron stays in tact

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65
Q

What is axonotmesis?

A

Axon is cut and the distal part is lost via Wallerian degeneration

Nerve can regrow back to original target (takes months)

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66
Q

What is neurotmesis?

A

Loss of axon and surrounding wrappings (endoneurium, perineurium, epineurium)

Poor prognosis, surgery may help

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67
Q

What is disrupted in neurotmesis?

A

Wrappings of the nerve beyond the myelin (endoneurium, perineurium, and/or epineurium)

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68
Q

What can you see in nerve conduction studies/electromyography in demyelination?

A

Decreased conduction velocity

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69
Q

What do you see in nerve conduction studies/electromyography in axonal loss?

A

decreased action potential amplitude

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70
Q

What occurs during wallerian degeneration?

A

Intra-axonal organelle and microtubule breakdown (mins-hours)

Schwann cells begin breakdown of axons and recruit macrophages

Macrophages do their thing

Then the path is cleared for axons to regrow from proximal to distal

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71
Q

Which is more conducive to nerve regeneration, CNS/PNS?

A

PNS

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72
Q

Does Wallerian degeneration occur in the PNS? CNS?

A

PNS only!

Oligodendrocytes not as good at initiating degradation as Schwann cells

CNS - astrocytes and microglia not as helpful as macrophages

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73
Q

Which cells (PNS/CNS) have greater intrinsic growth potential and why?

A

PNS cells - have greater expression of regeneration-associated genes (RAGs)

PNS neurons possess receptors and signal transduction machinery allowing them to grow in response to neurotrophins - retrograde injury signals

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74
Q

What are neurotrophins?

A

Retrograde injury signals - promote growth towards higher concnetration

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75
Q

What is a growth cone?

A

Very tip of a regenerating axon - sense the milieu and decide to grow or not (sense neurotrophins, for instance) and direct growth of axon

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76
Q

What is the molecular basis of a growth cone?

A

Cytoskeletal rearrangement - actin bundles and microtubules

Attachment of cytoskeleton to the signal transduction machinery is key

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77
Q

What are retraction bulbs (of Cajal)?

A

Failed regeneration growth cones of the CNS

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78
Q

What types of changes are seen in CNS plasticity?

A

Molecular and structural changes

Molecular include synapse, receptor, transmitter regulation

Help adapt instead of regrowing in CNS

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79
Q

What opportunities arise from the complexity of neuronal connetions in the brain?

A

Complexity allows for recovery in the case of injury - you can reroute or use other mechanisms - don’t have to fix the original pathway

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80
Q

How does activity help lead to neuronal plasticity?

A

Leads to increases in grwoth factors, especially BDNF (important in exercise)

Leading to increased neurogenesis, glial cell support.

Also, angiogenesis, synaptogenesis

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81
Q

What parallels are there between normal brain developmenta nd recovery from injury?

A

Birth->child age -> maturity

Injury->regrowth->consolidation

You need to prune the neuronal connections

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82
Q

What types of activities are best for helping regrow/recover from neuronal injuries?

A

A variety of skilled, task-specific, repetitive tasks - these are better than general exercise alone

e.g. real life skills (reaching into cupboard)

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83
Q

What are natural sources for stem cells?

A

Embryonic - inner cell mass from 4-5d blastocyst - usually from excess IVF cells - plurpotent

Fetal - from extra-fetal or fetal tissue (amniotic, cord blood, placental tissue) - multipotent

Adult - from BM, skin, GI, fat, heart, brain, dental pulp - multipotent or oligopotent - huge advantage is they are autologous

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84
Q

What is a difference between adult, fetal and embryonic stem cells?

A

adult - oligo or multipotent - autologous

fetal - multipotent

embryonic - pluripotent

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85
Q

What is somatic cell nuclear transfer?

A

Take nucleus from adult somatic cell and insert it into enucleated egg cell - get early embryo

Not 100% autologous - mitochondrial genome is still present

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86
Q

What are induced pluripotent stem cells (iPS) and their advantages?

A

Turn on four genes - myc, sox, oct, nanog - in a somatic cell and you get a stem cell

Pluripotent

100% autologous

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87
Q

What are the best targets for stem cel therapies?

A

Neurodegenerative diseases - Huntington’s (one type of neuron, isolated), ALS, Parkinson’s, Alzheimers (but it is very diffuse)

Stroke

Traumatic Brain Injury, Spinal Cord Injury

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88
Q

How many approved indications are there for pluripotent stem cells?

A

ZERO

Hematopoeitic stemm cells are used in bone marrow transplants

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89
Q

What are dysmyelinating diseases?

A

Disease where myelin sheath is abnormally formed (mostly related to inherited metabolic disorders)

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90
Q

What are demyelinating diseases?

A

Disease wher ethe myelin sheath is normally formed but is the target of destruction (e.g. MS)

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91
Q

What cells comprise the gray matter?

A

Neuron cell bodies

Dendrites

Synapses

Axons

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92
Q

What comprises the white matter?

A

Myelinated axons

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93
Q

What makes up the myelin of the CNS?

A

Oligodendroglial cells wrapped around the axon

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94
Q

Where in the brain are grey and white matter generally located?

A

Cortex - grey matter

Tracts underneath - white matter (including corpus callosum)

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95
Q

What are examples of dysmyelinating diseases?

A

Adrenoleukodystrophy - primarily affects white matter

Tay Sachs disease - primarily involves ccumulation of myelin byproducts in neurons

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96
Q

What is the general course of MS?

A

Initially begins with relapse/recover periods (something like IBD)

Then morphs into a progressive disease (something like Alzheimers)

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97
Q

What is multiple sclerosis?

A

Inflammatory, autoimmune disease of CNS

Characterized by relapsing neurologic symptoms, and progressive impairement of function

Variable symptoms and signs - monocular vision loss, brainstem, motor/sensory impairments, imbalance

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98
Q

What are common early features of MS?

A

Motor weakness, parasthesias, impaired vision, double vision, intention tremor, ataxia

These are symptoms common of other diseases, so you must work it up or look back at it later

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99
Q

What is Charcot’s triad?

A

Intention tremmor, nystagmus, scanning speech

Points to white matter pathways to and from cerebellum (vulnerable to demyelination)

Common presentation of MS

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100
Q

What is the most common form of involvement of the visual pathway of MS?

A

optic neuritis

Inflammation of optic nerve - painful

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101
Q

What is a very common first presenting feature of MS?

A

Optic neuritis - inflammation of optic nerve - presents with pain

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102
Q

What type of eye involvement is common in MS?

A

Optic neuritis - painful upon movement

Common to have a scotoma - isolated area of visual field with absent vision

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103
Q

What is the prognosis of optic neuritis that is seen early in MS?

A

1/3 will recover completely, the rest will improve substantially

Half of patients who present with optic neuritis alone will develop other signs of MS

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104
Q

What is RR-MS?

A

Relapsing-remitting MS

Relapses, recovery, and stability between

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105
Q

What are the different clinical patterns of MS?

A

Relapsing-remitting, secondary progressive, primary progressive, progressive relapsing

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106
Q

What is secondary progressive MS?

A

Relapse with recovery, then gradual worsening of symptoms over time

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107
Q

What is primary progressive MS?

A

gradual worsening of symptoms - no cardinal features of relapses

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108
Q

What is the relationship between brain lesions and disability in MS?

A

We can see lesions more readily than attacks, and are indicators of progression of MS

Looking below the surface of symptoms reveals worsening picture of lesions in the brain

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109
Q

What is clinically isolated syndrome?

A

First presentation of what is liekly to become MS - (singular sclerosis)

Within 10 years, 50% wil develop secondary-progressive MS

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110
Q

Who gets MS?

A

young people: 20-40 (big spread)

Particularly women (3:1)

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111
Q

What is the most common cause of medical disability in young adults?

A

MS

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112
Q

In what ethnicity is MS more common?

A

North European descent

Seen more common in latitudes further from equator too

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113
Q

What are the genetic fators of MS?

A

Complex - but twins at 30% chance of getting MS, siblings 2-5%

Both more common than general population

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114
Q

What helps you make the diagnosis for MS?

A

Dissemination in space and time of disease activity

Based on history and neurological exam

No single diagnostic test

MRI can help

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115
Q

What is the significance of contrast-enhanced lesions in the brain on MRI?

A

Indicate active inflammation. Lesion associated with MS

In non-contrast MRI - indicate history of MS lesions

116
Q

In non-contrast-enhacned MRI, what is the significant of lesions in white matter tracts?

A

Old MS plaques. Active inflammation can be seen by contrast enhancement

117
Q

What is this MRI indicative of?

A

Multiple Sclerosis

Periventricular lesions - radiating upward and outward from ventricles + white matter tracts

Radiating upwards from corpus callosum

Brainstem, cerebellum lesions

118
Q

How do MRI lesions predict development of MS after presentation with optic neuritis (or other first attack)?

A

Increased likelihood

119
Q

What must you be sure of before diagnosing MS?

A

That there is no better explanation, e.g.:

 Infectious: Lyme, Syphilis, HIV, HTLV-1, PML

 Inflammatory: SLE, Sjogren’s syndrome, vasculitis,

sarcoidosis, Bechet’s syndrome, APLS

 Metabolic: Vitamin B12 deficiency, dysmyelinating

diseases (lysosomal/leukodystrophies), toxins, CPM,

mitochrondrial disorders, Copper deficiency,

 Vascular: CADASIL, susac’s syndrome

 Neoplastic: CNS lymphoma, metastatic disease

 Structural Spine disease: AVMs, degenerative disc

disease, syrinx, arnold-chiari

 Genetic- hereditary spastic paraparesis

Psychogenic-Depression, anxiety, conversion

120
Q

What occurs from an immunological perspective in Multiple Sclerosis?

A

Th1 cells become activated and self-reactive T cells enter brain and mistake myelin for antigens

Without regulatory cells, they are reactivated and release proinflammatory cytokines that increase inflammation, cause edema, and damage myelin and nerves

121
Q

What type of disregulation is thought to occur in MS with respect to Th cells?

A

Th1 more than Th2 (inflammatory more than anti-inflammatory)

122
Q

What do you see in the CSF of MS patients?

A

Oligoclonal bands - identified by electrophoresis of CSF

Two or more bands needed to be seen for it to be useful

IgG bands

123
Q

What are oligoclonal bands?

A

When you electrophorese CSF in MS patients, you will see excess of bands instead of smear, of IgG

124
Q

What is seen in histological sections of MS lesions?

A

Peri-venular inflammatory infiltrates

125
Q

What are the goals of treating MS?

A

Treat relapses and exacerbation

Prevent relapses

Reduce devleopment of disability

Treat symptoms

126
Q

What can be used to directly treat MS relapses/exacerbations?

A

High dose IV steroids - remember, this is an inflammatory event.

127
Q

What are some limitations of treating MS?

A

Disease modifying agents are only partially effective

All injectible (IV)

Side effects of interferons (flu-like, headche, fever)

Risk/Benefit

128
Q

How can you identify an acute exacerbation of MS that you should treat?

A

Must distinguish from Uhthoff’s phenomenon (which is sudden onset of neurological dysfunction as a result of elevated body temperature)

Episode of neurological dysfunction lasting more than 24 hours in the absence of fever or infection

129
Q

What is Uhthoff’s phenomenon?

A

A sudden onset of neurological dysfunction as a result of elevated body temperature

130
Q

What drug do you use to treat acute exacerbations of MS?

A

IV methylprednisone - high dose

131
Q

What are common causes of head injury?

A

Motor vehicle crash

Pedestrian Accidents

Assault

Falls

Gunshot or stab wounds

Occupational

Child abuse

132
Q

How do you diagnose head injury?

A

Examine the patient’s level of consciousness, motor response, pupillary light response, ability to talk (orientation), ability to breathe

133
Q

What is used to assess degree of head trauma?

A

Glasgow Coma Scale - correlates with outcome (lower scores = worse outcomes)

134
Q

What defines a mild head injury?

A

GCS 13-15 (glasgow coma scale)

135
Q

What defines a moderate head injury?

A

GCS 9-12 (glasgow coma scale)

136
Q

What defines a severe head injury?

A

GCS 3-8 (glasgow coma scale)

137
Q

What tests are done for most patients with head injury?

A

X-rays (but nowadays more commonly CT scans)

CT can detect blood in and around brain acutely; fractures; is easy and quick; Gold Standard

138
Q

What is the gold standard in acute head injury diagnosis?

A

CT scan

139
Q

What is wrong here?

A

Depressed skull fracture

140
Q

What occurs in an epidural hematoma?

A

Fracture causes rupture of middle meningeal artery, causing blood accumulation between calvarium and dura

May cause uncal herniation

Lucid interval - recover quickly from concussion, but then are fine until the hematoma causes you to further problems

141
Q

What is wrong here?

A

Epidural hematoma

142
Q

What occurs in subdural hematoma?

A

Blood accumulation between dura and pia/arachnoid layer. Bridging veins are sheared during acceleration/deceleration injury

143
Q

What is a difference between the localization of a subdural and epidural hematoma?

A

Epidural - the brain sutures prove to be too strong of attachments for the dura - blood does not pass beyond them

Subdural - below dura, so there are no restrictions of where blood can go

144
Q

What occurs in the progression of a subdural hematoma?

A

Acute - can visibly see crescent shaped lesion.

Subacute - harder to see, spreads out

Chronic - hypodensities and thickening and mixed-age images

145
Q

What are cerebral contusions?

A

Intra-parenchymal lesions

146
Q

Where are cerebral contusions more likely to be found?

A

Frontal and temporal lobes - they can get caught in wings of sphenoid bone or in the ridges of the roof of the orbit

Particularly during accelerations/deccelerations

147
Q

What is the most common cause of subarachnoid hemmorrhage?

A

Trauma

148
Q

What is a coup injury?

A

Injury on the side of the impact

Counter-coup is on the opposite side

149
Q

What is a counter-coup injury?

A

Injury on the opposite side to that of impact

Coup injury is that on the same side

150
Q

What defines a concussion?

A

transient alteration of consciousness due to an impact to the head

Temporary alteration of ion channels and energy balance

Can be associated with normal head CT

151
Q

What are the diffuse brain injuries?

A

Concussion

Diffuse Axonal Injury

152
Q

What is diffuse axonal injury?

A

longer periods of unconsciousness or coma

CT scan is often normal or with evidence of punctate hemorrhages within grey/white junctions

Exam may be disproportionate to radiographic appearance

153
Q

What are clinical signs of concussion?

A

Confusion

Amnesia (retrograde or anterograde)

May report “seeing stars” or “white/black out” visually

154
Q

What is post-concussion syndrome?

A

Often resolves within a few days or weeks, but can persist for months

Symptoms: Headache, N/V, dizziness, visual complaints, fatigue, depression, difficulty concentrating, reading, memory, insomnia, sleeping more

155
Q

What is chronic traumatic encephalopathy (CTE)?

A

Repetitive brain injury (dementia pugilistica - boxers; but seen in other sports i.e. football)

Possible repetitive axonal stretching and deformation - especially in those with unresolved concussive events

156
Q

What can you see in gross pathology in CTE patients?

A

Atrophy - general cortical;mesial temporal/mammillary bodies

Cavum septum pellucidum - septal fenestrations

Pallor - locus ceruleus/substantia nigra

157
Q

What is this patient likely to have suffered from?

A

Chronic Traumatic Encephalopathy

158
Q

What do you see on a molecular level in chronic traumatic encephalopathy?

A

Tau-protein immunoreactivity (but more in cortical layers and sulci vs in AD)

Also found perivascularly, in mammillary bodies, and hippocampus

β-amyloid plaque formation is less consistently found than in AD

159
Q

What are clinical features of CTE patients?

A

Early - short term memory impairment; cognitive dysfunction; depression/emotional instability; impulse control problems; suicidality

Late - Dementia; Parkinsonism

160
Q

What are potential genetic risk factors for CTE?

A

Apolipoprotein E allele 4

161
Q

What is severe head injury defined by?

A

Glasgow Coma score 3-8

must ensure your ABCs!

162
Q

What is done to a patient with a severe head injury?

A

Place patient on ventilator

Place monitor ot measure brain pressure (ICP)

Perform surgery on any large hematomas within brain for significant swelling

163
Q

Why is ICP monitoring important in severe head injury?

A

Allows for early warning for significant intracranial developments

Enables cerebral perfusion pressure measurement

164
Q

What is the cerebral perfusion pressure?

A

CPP = MAP - ICP

(Inflow - outflow)

165
Q

What are contributors to the ICP?

A

Cranial vault which is a closed cavity

The three components therein - brain, blood, CSF

166
Q

What is the Monro-Kellie Doctrine?

A

Calvarium is a fixed volume - increases in volume wil cause increasingly bigger increases in pressure

167
Q

What is the primary injury in severe head injury?

A

Moment of impact - irreversible

168
Q

What is the secondary injury in severe head injury?

A

Anytime after primary impact - especially first 24 hours and preventible, mostly

ISCHEMIA

169
Q

What are causes of ischemia in head injury?

A

Decreased perfusion due to high ICP (due to hemorrhage/edema)

Hypoxia

Hyoptension

170
Q

What are the biochemical changes in ischemia?

A

Influx of calcium - calcium release from ER due to decreased ATP, increase in glutamate release, due to increased activation of NMDA Ca++ channels

171
Q

What is Poiseulle’s Law?

A

Q = flow

P = Transmural pressure gradient

r = radius

l = length

η = viscosity

172
Q

What is normal cerebral blood flow?

A

50 cc/100g/min

173
Q

What is cerebral blood flow in reversible ischemia?

A

10-20 cc/100g/min

174
Q

What is cerebral blood flow in irreversible ischemia?

A

<10 cc/100g/min

175
Q

What is brain oxygen monitoring useful for?

A

Early indication of ischemic events

Variable correlation with SjvO2 - good correlation with global insults

CPP < 60 with negative effect

BTPO2 < 15-20 mmHg = impending hypoxia

BTPO2 < 10 mmHg = hypoxia and increased glutamate seen

176
Q

What can help prevent secondary injury in severe head injuries?

A

Maintaining good oxygen delivery to brain cells

177
Q

What is the basis for most classifications of psychiatric illnesses?

A

Clinical observation and symptom description

178
Q

Is the etiology of any psychiatric disorder known?

A

No

Limited understanding of pathyphysiology

179
Q

What is automaticity?

A

Unconscious mental activity directs behavior, thoughts, feelings.

You respond before you know you’re responding

180
Q

What does non-conscious mean?

A

Mental functioning that is not represented in consciousness and of which one is unaware

(unconscious)

181
Q

What is unconsciousness?

A

Lack of consciousness or responsiveness to people and other environmental stimuli

182
Q

What is subliminal?

A

That which is below an individual’s threshold for conscious perception

183
Q

What is id?

A

Totally unconscious

Instincutal drives (sex, aggression, eating, power, physical contact)

Primary process that demands gratification and ignores reality

184
Q

What is ego?

A

Conscious and unconscious

Moderates between id and superego and seeks compromises to pacify both

Executive of the psyche, involved in regulatory functions

185
Q

What is superego?

A

Conscious and unconscious

Morals, conscience, internalized parents, self-criticism

Denies gratification

186
Q

What is psychodynamics?

A

Concept that unconscious mental life directs behavior, thoughts, feelings, responses, etc

Parts of the mind are in conflict

The mind regulates or disavows experiences to preserve equilibrium and avoid dissonance

Past being alive in the present and relationship patterns being repeated

Symptoms have meaning/purpose to a patient

Psychodynamic psychotherapy helps us recognize the ways in which we disavow aspects of our experience so as to permit us to have more choice in present situations.

187
Q

What is a defense mechanism?

A

This process of Implicit Emotion Regulation is provided by Defense Mechanisms, whereby people unconsciously adjust perceptions/experiences to preserve equilibrium, protect self- esteem, avoid more severe aversive feelings, etc.

Distort one’s representation of reality to create emotionally preferable conclusions & determine what reaches awareness

188
Q

When are defense mechanisms pathological?

A

When there is a rigid use of a limited repertoire of defenses

When they are immature or maladaptive

189
Q

What is repression?

A

Blocking ideas/impulses from conscious mind

190
Q

What is forgetting?

A

Repression of an emotion that manifests as forgetting

191
Q

What is altruism?

A

Unselfishness in response to unconcsiously distressing feelings

Unselfishness to maintain consistent sense of self

192
Q

What is humor?

A

unconsciously dealing with distressing feeling/thought by joking (more maladaptive if resentment, hostility)

193
Q

What is suppression?

A

Consciously pushing a thought or feeling out of awareness

194
Q

What is sublimation?

A

Expressing a socially or personally unacceptable feeling or thought in an acceptible way

195
Q

What is displacement?

A

Directing the object of one’s feelings to a safer one

196
Q

What is rationalization?

A

making excuses

Dealing with emotional distress or internal/external stressors by concealing the true motivations for one’s own thoughts, actions, or feelings through making reassuring but incorrect explanations

197
Q

What is intellectualization?

A

Using excessive and abstract thinking to avoid difficult feelings

Flight into reason

Involves emotionally removing one’s self from a stressful event

A person studies or works to explain something rather than to have an understandable emotional reaction to it

198
Q

What is isolation of affect?

A

Remainig aware of the descriptive details of an event but losing connection with the feelings about the event

199
Q

What is identification with the aggressor?

A

Reversing the power roles

Instead of being object of threat, you become the one making the threat; allowing the victim to achieve some feeling of strength in an otherwise humiliating/painful situation

stockholm syndrome

200
Q

What is reaction formation?

A

Your behaviors, thoughts or feelings are the complete opposite of your unconscious desires/etc

201
Q

What is somatization?

A

Directing intolerable thoughts or feelings towards your body

202
Q

What are mature defenses? vs immature?

A

Allow flexible adaptation to reality, cognitively complex

immature distort reality

203
Q

What are immature defenses? vs mature ones?

A

Distort reality, appear early, maladaptive residues of childhood experiences

vs cognitively complex defenses that allow flexible adaptation

204
Q

What is acting out?

A

Dealing with emotional distress by actions rather than reflection or words

Primitive defense

205
Q

What is splitting?

A

Primitive defense

Compartmentalizing internal representations of self and others into all-good and all-bad so that conflict is avoided

206
Q

What is projection?

A

primitive defense

To avoid ownign an intolerable thought or feeling, a person attributes it to another person

207
Q

What is projective identification?

A

primitive defense mechanism

Defense involving subtle interpersonal pressure so that the target of a projection takes on characteristics of that which is being projected

208
Q

What is denial?

A

Primitive defense mechanism

By dismissing perceptions that are obvious to everyone in the environment, the person avoids awareness of aspects of external realities that are difficult to face

209
Q

What is withdrawal?

A

Primitive defense

Retreating into one’s private internal world to avoid anxiety about interpersonal situations

210
Q

What is dissociation?

A

Primitive defense mechanism

Separating off parts of ones self to avoid acknowledgement of distressing experiences

211
Q

Who uses defenses?

A

Everyone

They are not necessarily unhealthy

212
Q

What is transference?

A

The unconscious transfer of past relationship patterns onto someone in the present

Emotionally charged interpersonal memories hold center court

Both conscious and subliminal present stimuli activate such procedural memory traces and shape present perception

The neural signature of an activated memory can be similar to that of true external stimuli

213
Q

What is concordant countertransferance?

A

One person experiences another’s feelings (empathy)

214
Q

What is complementary countertransferance?

A

Person experiences feelings similar to what other people in the other person’s life have felt in response to that peson

Role responsiveness

215
Q

What is the diagnostic criteria for major depressive disorder?

A

At least 5 symptoms present for at least 2 weeks and impair function:

Sad mood*

Anhedonia*

Sleep disturbance

Change in appetite

Low energy/fatigue

Psychomotor agitation or retardation

Impaired concentration

Guilty feelings, self blame

Suicidal/thoughts of death

*Need one of these two for a diagnosis

216
Q

What are symptoms that must be present for a diagnosis of major depressive disorder?

A

One of:

Sad mood
Anhedonia

217
Q

How do you screen for depresion?

A

PHQ-9

PHQ-2 (preliminary, if positive, do PHQ-9)

218
Q

What is the gender that suffers from major depressive disorder more commonly?

A

Females (2x as common)

219
Q

What is the course of illness in major depressive disorder?

A

May be triggered by an event

Untreated may last 6-13 months; treated last 3 months

Tends to be chronic with relapses - previous episodes increase risk of future episodes

220
Q

What are consequences of untreated or undertreated major depressive disorder?

A

Suicide (30% attempt, 15% complete)

Divorce or relationship issues

Decreased productivity/ability to work

Poor hygiene

Can’t care for children

Decreased quality of life

Effects on caregivers

Medical comorbidities

221
Q

What is the psychodynamic theory of depression?

A

Disturbances in infant-mother relationship during oral phase causes damaged self esteem and unresolved conflict from real or imagined object loss

Anger toward lost object turns inward

Goal of treatment should be symptom relief and personality change through understanding of unconscious conflicts

222
Q

What is the cognitive theory of depression?

A

Depression results from specific cognitive distoritons

Learned negative views about self, environment and future

Treat with cognitive behavioral therapy

223
Q

What are neurobiological theories of depression?

A

Monoamine deficiency hypothesis

Amino acid neurotransmiter system dysregulation

Neuroendocrine dysregulation

Structural and functional brain changes

Neuropathological changes

Impairments in neuroplasticity

224
Q

What is the monoamine deficiency hypothesis of depression?

A

Early antidepressants block reuptake or degradation of serotonin and norepinephrine

Led to belief that depression resulted from deficiency of monamines

Studies have yet to reliably demonstrate this - depletion of monoamines doesn’t cause depression in healthy subjects; Also, antidepressants take 4-6 weeks for clinical benefit, but work to increase monoamine transmission instantly

225
Q

What is the glutamate dysfunction theory of depression?

A

Chronic stress = excess glutamate

Hyperactivation of NMDA type glutamate receptors on neurons and glial cells

End result is atrophy and death of neurons and glial cells

IV ketamine (NMDA antagonist) has rapid antidepressant effect

226
Q

What is the neuroendocrine theory of depression?

A

Excess cortisol present - can have damage to brain areas (hippocampus -atrophy)

Decreased supression of hypothalamus and anterior pituitary (decreased negative feedback effect)

227
Q

What is the dexamethasone test?

A

Test where you give exogenous steroid in order to attempt to induce the negative feedback fo HPA axis to test its functionality

Not specific or sensitive for depression, but about 50% of patients with depression will fail the test

228
Q

What happens to your hippocampal volume the longer you go with untreated depression?

A

Decreases!

229
Q

What are brain changes in depression?

A

Structural: decreased volume of hippocampus, dorsolateral PFC, anterior cingulate, amygdala, OFC

Functional: decerased anterior cingulate, dorsolateral PFC activity; increased amygdala, orbitofrontal cortex activity

Relative lack of cortical regulation of the limbic system during adversity

230
Q

What is the most prominent feature of cell pathology in depression?

A

Reduction in glial cell density and number

Seen in orbital cortex, dorsolateral PFC, anterior cingulate, hippocampus, amygdala

231
Q

What is BDNF?

A

Brain-derived neurotrophic factor

Important for axonal growth, neuronal survival, and for synaptic plasticity

BDNF levels affected by stress and cortisol

232
Q

What is the relationship between BDNF and sensitivity to stress in healthy people?

A

Inverse correlation

Low BDNF found in hippocampus, PFC and serum of depressed patients

Polymorphism in BDNF gene may be associated with hippocampal hypersensitivity to stress and increased vulnerability to depression

233
Q

What is the neurotrophic hypothesis of depression?

A

Depression may be in part cuased by decrease in neurotrophic factors and the subsequent failure of neuronal plasticity

Enhancement in neural plasticity and cellular resilience is final common pathway for all effective therapies

234
Q

What are the genetics of depression?

A

It is 37% heritable

No single depression gene

Gene x environment

Epigenetics may play a role

235
Q

What are treatments for depression?

A

Medications - SSRIs, Tricyclics, Monoamine oxidase inhibitors, others

Psychotherapy

Electroconvulsive Therapy (80% response)

Vagal Nerve stimulation

236
Q

What are the diagnostic criteria for bipolar I disorder?

A

At least one week of abnormally and persistently elevated, expansive, or irritable mood

PLUS 3 or more of:

Inflated self esteem/grandiosity
Decreased need for sleep

More talkative

Flight of ideas/racing thoughts

Distractibility
Increased goal-directed activity/psychomotor agitation

Excessive involvement in pleasurable activities with high potential for painful consequences

Impaired functioning/need for hospitalizaiton

237
Q

What is the lifetime prevalence of Bipolar I disorder?

A

0.5-1% (less than depression)

238
Q

What gender is more commonly afflicted with bipolar I disorder?

A

Equal in men and women

239
Q

What is the typical range of onset of bipolar I disorder?

A

18-44 (typically on the younger end)

240
Q

What is the neurobiology of bipolar disorder?

A

Structural and functional changes (dysregulation in limbic and PFC circuitry)

Endocrine (HPA/HPT axis dysregulation)

Cellular (decreased neuronal size and density in key areas)

241
Q

What are the genetics of bipolar disorder?

A

8-10x increased risk of bipolar disorder in first degree relatives of bipolar individuals

2-10x increased risk of major depressive disorder in first degree relatives of bipolar individuals

65% heritable - no genes found yet

242
Q

What demographic has the highest rates of suicide?

A

Men older than 75

243
Q

What are risk factors for suicide?

A

Family history

Demographics - older white males

Previous attempts

Psychiatric disorders

Substance abuse

Chronic pain, illness, etc

244
Q

What are protective factors for suicide?

A

Good clinical care

Easy access to clinical interventions, support

Connectedness

Religion

Skills in problem solving

Children

245
Q

What are things that are important in the development of resilience (10)?

A

Positive attitude, optimism

Cognitive flexibility through cognitive reappraisal - reframe, assimilate, accept and recover from stress. Failure is essential for growth

Embrace a personal moral compass - develop core set of beliefs that few things can shatter; Altruism is strongly related to resilience

Find a resilient role model

Face your fears

Develop active coping skills

Establish and nurture a supportive social network

Attend to physical well being

Train regularly and rigorously in multiple areas

Recognize, utilize, and foster signature strengths

246
Q

What is the stockdale paradox?

A

Retaining faith that you will prevail in the end, regardless of the difficulties, while at the same time confronting the most brutal facts of your current reality, whatever they might be

247
Q

Which sex gets anxiety disorders more commonly?

A

Females

248
Q

What are the anxiety disorders?

A
  • Panic Disorder with/without Agoraphobia
  • Social Anxiety Disorder
  • Generalized Anxiety Disorder
  • SpecificPhobia
  • Separation Anxiety Disorder
  • SelectiveMutism
  • Substance/Medication Induced Anxiety Disorder
  • Anxiety Disorder due to Medical Condition
249
Q

What is the most common anxiety disorder?

A

Specific phobia

250
Q

What are subjective symptoms common to all anxiety disorders?

A

Apprehension

Worry

Anticipation

Fear

Hypervigilence

Restlessness

Impaired concentration

Depression

251
Q

What are physiological symptoms common to all anxiety disorders?

A

Neuromuscular (tension, fatigue, tremor)

GI - dry mouth, difficulty swallowing

Hyperventilation

Cardiovascular (palpitations)

252
Q

What is Panic Disorder?

A

Recurrent, unexpected panic attacks

Anticipatory anxiety - more than 1 month of concern about having additional attacks, worrying about their implications, or change in behavior related to anticipatory anxiety (avoidance)

Not attributable to substance or another medical condition

+/- Agoraphobia (Fear or avoidance of situations from which escape might be difficult/embarrassing or in which help might not be readily available if have panic attack)

253
Q

What is agoraphobia?

A

Fear or avoidance of situations from which escape might be difficult/embarrassing or in which help might not be readily available if have panic attack

254
Q

What is a panic attack?

A

Abrupt surge of intense fear that builds ot crescendo pattern

Sudden onset, peaks within minutes, lasts 5-30 minutes

Often out of the blue, presents with physical symptoms

Emotional symptoms of fear of dying, or losing control

Can occur in non-physiologically ill people

Can occur in other disorders besides panic disorder

255
Q

What are physical symptoms of panic attacks?

A

Hyperventilation

Palpitations
Sweating
Trembling or shaking
Feelings of choking
Chest pain or discomfort

Nausea or abdominal distress

Parasthesias

Chills or hot flashes

Derealization or depersonalization

Dizzy, unsteady, lighteaded, syncope

Dyspnea or air hunger, frequent sighing

256
Q

What is the cardianl symptom of panic?

A

Hyperventilation

257
Q

What is significant about hyperventilation and panic?

A

Cardinal symptom

Panic patients are chronic hyperventilators who also acutely hyperventialte during panic attacks

Hyperventilation -> hypocapnia (reduced CO2) and alkalosis -> decreased cerebral blood flow -> dizziness, confusion, derealizaiton.

258
Q

What is the epidemiology of panic disorder?

A

Females > males (2-3:1)

Young adults in 3rd decade more commonly, but can be later

Women during childbearing years

259
Q

What is the course of panic disorder?

A

Highly variable

– 30-40% symptom free

– 50% mild symptoms

– 10-20% significant symptoms

Ideal is to treat panic attacks before you get phobic avoidance - often leads to complete remission

Can lead to suicidality

260
Q

What are common comorbidities with panic disorder?

A

Major depressive disorder

Other anxiety disorders

Alcohol (in 20%) and other substance dependence

Medical unexplained syndromes

Other medical conditions (peptic ulcer disease, asthma, migraines, HTN)

261
Q

What is generalized anxiety disorder (GAD)?

A

Excessive anxiety and worry, most days, for at least six months

Difficult to control the worry

At least three of:

  • restlessness/keyed up
  • poor concentration
  • muscle tension
  • easily fatigued
  • irritability
  • sleep disturbance

That leads to impaired functioning

262
Q

What gender is afflicted by generalized anxiety disorder more?

A

Females

263
Q

When is generalized anxiety disorder typically onset?

A

early 20s but can develop at any age

264
Q

What is social phobia (social anxiety disorder)?

A

Fear of 1 or more social or performance situations in which exposed to unfamiliar people or to possible scrutiny by others

Exposure to feared situation provokes anxiety

Fear or anxiety is out of proportion to actual threat

Tend to avoid situations or endure with intense anxiety

Causes functional impairment

Lasts at least 6 months

265
Q

What are typical fears of social phobia?

A

Fear of speaking

Fear of meeting people

Fear of eating in public

Fear of using public phone

Fear of using public bathroom

Fear of attending parties

266
Q

What is the basis for the fear in social phobia?

A

Fear of appearing nervous or foolish

Fear of being embarrassed/humiliated

Fear of making mistakes

Fear of beign criticized

Fear of being laughed at

Fear that actions will lead to being rejected or offending others

267
Q

What is the gender distribution of social phobia?

A

No difference between men and women

268
Q

Which anxiety disorder shows no gender bias?

A

Social phobia

269
Q

When is the typical onset of social phobia?

A

Late childhood/early adolescence

Can be acute, following humiliating social experience; or can be insiduous

270
Q

What is the course and outcome of social phobia?

A

Can be asymptomatic unless confronted with phobic situation or can be demoralizing, isolating and disabling vocational and interpersonal impairments

271
Q

What is the key to treating anxiety disorders?

A

Cognitive Behavroral Therapy

In concert with medications

272
Q

What are the cognitive-behavioral theories of anxiety disorders?

A

Learned response from parental behavior

Classical conditioning

Faulty thinking patterns, catastrophic thinking, accompany or precede maladaptive behaviors and emotional disorders

273
Q

What neurobiological factors are implicated in anxiety disorders?

A

Disordered fear circuitry

False suffocation/abnormal sensitivity

Neurotransmitter abnormalities

Structural and functional brain changes

Genetics

274
Q

What may be the neurobiological basis of panic?

A

Abnormally sensitive fear network (PFC, thalamus, insula, amygdala, amygdalar projections to brainstem and hypothalamus)

Potential deficit in cortical processing pathways -> misinterpretation of sensory information -> inappropriate activaiton of fear network

275
Q

What is the role of the hippocampus in panic?

A

Formation of contextual memory

May be important for phobic avoidance, whcih in part arises from an association of panic attacks with teh context in which they occurred

276
Q

What are neurotransmitters implicated in panic disorder?

A

Serotonin

Norepinephrine

GABA

277
Q

What evidence exists to support the theory that serotonergic dysfunction is important in panic disorder?

A

SSRIs treat panic disorder

Decreased 5HT1A receptor binding in cingulate cortex and raphe nucleus

Works on downstream sites to dampen autonomic arousal:

278
Q

What evidence is there to suggest that there is noradrenergic dysregulation in panic disorder?

A

Increased noradrenergic transmission from locus ceruleus

Increased NE concentrations in serum cause panic/anxiety

Panic disorder associated with increased activity and sensitivity of noradrenergic system

279
Q

What evidence is there to suggest that GABA is important in panic?

A

Decreased benzodiazepine receptor binding to GABA-A receptor in hippocampus and amygdala in panic disorder may imply fewer GABA-A receptors or a decreased sensitivity of the receptors

Lower concentrations of cortical GABA in panic disorder patients vs controls

280
Q

What is the genetics of anxiety disorders?

A

Genes contribute, but environmental influences are substantial

Complex non-mendelian inheritance

Maybe you inherit the tendency for fearfulness/susceptibility to panic

281
Q

What is behavioral inhibition?

A

Reticence when faced with novel situations/people

Linked to risk for social phobia and other anxiety disorders

282
Q

What are environmental contributors to anxiety disorders?

A

Disruption of early attachment and childhool trauma may be associated with later development of panic disorder

Those with panic disorder may be more susceptible to the effects of trauma than those without

80% of patients with panic disorder report major stressor in previous 12 months

Interaction b/w life stress + genetic susceptibility that contributes to panic disorder

283
Q

How do you treat anxiety disorders pharmacologically?

A

SSRIs, SNRIs

Tricyclic antidepressatns, MAOIs

Benzodiazepines

Anticonvulsants

However, often found to be very sensitive to side effects of these drugs

284
Q

What are non-pharmacological therapies for panic disorders?

A

Cognitive Behavioral Therapy

Robust and effective treatment

Psychoeducation about panic to correct misconceptions

Cognitive restructuring to identify and correct distortions in thinking

Exposure to feared bodily sensation and situations

285
Q

How does CBT work to treat panic?

A

Operates upstream from amygdala

Strengthens ability of cortical projections to assert reason over (and inhibit) automatic behavioral and physical responses

286
Q

Anxiety disorders might be characterized by […] of subcortical emotion-processing areas and hypoactivity of cognitive processing/”top-down control” areas

A

Anxiety disorders might be characterized by hyperactivity of subcortical emotion-processing areas and hypoactivity of cognitive processing/”top-down control” areas

287
Q

Anxiety disorders might be characterized by hyperactivity of subcortical emotion-processing areas and […] of cognitive processing/”top-down control” areas

A

Anxiety disorders might be characterized by hyperactivity of subcortical emotion-processing areas and hypoactivity of cognitive processing/”top-down control” areas

Brain and Behavior (9 decks)

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