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Neuroscience Flashcards

1
Q

Tabes Dorsalis

A

Consequence of syphilitic infection. Destruction of DRG cells with LARGE diameter MYELINATED AXONS.
LOSS OF TOUCH AND PROPRIOCEPTION (bilaterally?)
Nociception and T remain almost unaffected.

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2
Q

Phantom Limb Sensations

A

Reorganisation of cortical maps post- losing a limb.
Phantom limb sensations can be evoked by touching the face - perceived as pain from parts of phantom limb.
Touch pathways in the face form new circuits, connect with neurons that would have become useless for arm.

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3
Q

Hyperalgesia

A

Enhanced sensitivity and responsively to stimulation in area surrounding damaged tissue.
Due to sensitisation of nociceptors - bc of chemical substances released within the damaged area ie Prostaglandins, leukotrienes, substance P (signalling substance of primary afferent pain fibres) is

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4
Q

Allodynia

A

Normally non-noxious stimuli cause sensation of pain ie putting on a shirt after sunburn

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5
Q

Classifications of pain

A

Nociceptive - activation of nociceptors

Neuropathic - due to aberrant somatosensory processing ie phantom limb pain

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6
Q

Angina Pectoris Referred pain

A

Metabolic Products of ischemia stimulate visceral pain fibres. Pass through spinal nerve roots between C7 and T4, with cutaneous fibres. CONVERGENCE on a secondary sensory neuron within the spinal cord

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7
Q

Where would the ALS and Medial lemniscus likely be injured together?

A

Come close together at pons and midbrain, could be lesioned together here - ie impaired point discrim, pain, T from R side of body.

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8
Q

If loss of pain and thermal sensation on R side of face, where is the lesion?

A

Has to be at medulla or above because if it were below, would have BILATERAL loss of pain and thermal sensation, since the Trigminal pain path descends to the spinal trigeminal nucleus and then ascends through the medulla and pons.

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9
Q

Noxious substances released from damaged tissues that activate nociceptors

A

Blood - bradykinin
Mast cells - histamine
Potassium from damaged cells (ischemia, MI)

  • activate nociceptors
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10
Q

Gate Control

A

In dorsal horn of spinal cord. Large myelinated fibres carrying touch sensations activate inhibitory interneurons within dorsal horn (interneuron releases ENKEPHALIN onto opioid receptors), reduce flow of nociceptive information through the gate between nociceptors (first order neurons of pain path) and their second order neurons.

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11
Q

Pain interventions

A

Inhibit sensitising agents ie prostaglandins
Inhibit pain pathway - ie block at DRG
Opioid drugs - increase interneurons activation inhibiting pain pathway ie codeine morphine, mimick enkephalin

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12
Q

Far Vision Accomodations

A 
Light rays are ~ PARALLEL
Cornea Refractive power 42 D (1/m)
LENS refractive power 13 D (1/m), flattened
CILIARY MUSCLE (circular): relaxed
SUSPENSORY LIGAMENTS: tightened
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13
Q

Near Vision Accomodation

A 
Light rays are NOT parallel. 
CILIARY MUSCLE (CIRCULAR) - CONSTRICTED
SUSPENSORY LIGAMENTS - SLACK
Cornea 42 D
Lens, more convex, increases to about 26 D in young person.
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14
Q

Presbyopia

A

Lens looses its elasticity in ageing - reducing ability to focus on near objects. Focal length is too great (not converged fast enough)
Correct with a CONVEX LENS (Reading glasses)

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15
Q

Visual Acuity

A

Ability to distinguish two nearby points. Visual acuity is HIGH when two-point discrimination threshold is LOW (High spatial resolution)
Depends on density of photoreceptors, and proper function of optical apparatus of eye ie accommodation - if optical apparatus fails, objects appear blurry.

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16
Q

Emmetropia

A

Sharp picture of parallel rays entering the eye - refractive power of optical apparatus matches the length of the eyeball. Normal sightedness.

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17
Q

Myopia

A

(Nearsightedness)
Focus of parallel light rays is ANTERIOR to photosensitive elements of retinal photoreceptors.
Objects closer to the eye can be focused even without usual accommodation. Vision is best for NEAR objects.
CORRECT WITH: CONCAVE LENS

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18
Q

Hyperopia

A

(Farsightedness)
Focus of light rays is beyond the retina when ciliary muscle is relaxed and lens has its lowest refractive power.
Distant objects can be focused by activating mechanisms for near accomodation, increasing refractive power
Fails for close objects, vision best for far objects.
CORRECTED USING CONVEX (+D) LENS

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19
Q

Papilledema

A

Indicates increased ICP. Seen on inspection of ocular fundus. Increased ICP compromises venous drainage - dilation of retinal veins.
Optic disc is pushed forward and disc appears white.

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20
Q

Detached Retina

A

Retina separates from RPE and areas detached lose their function.
Focal lesion in defined region causes scotoma - an area of vision loss.
Detached part of retina will NOT regain its function even with surgery.

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21
Q

Age Related Macular Degeneration (AMD)

A

Poor central vision. Number of genetic, enviro, age, smoking, BMI can contribute to incidence.
Cells of RPE atrophy and outer segment waste removal becomes less efficient.

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22
Q

Diabetic Retinopathy

A

Initial small scotomas often unrecognised. Once macula is involved, visual loss is dramatic.
Defects caused by blood supply dysfunction, reduction of permeability of basal membranes of capillary endothelial cells and bv damage (aneurysms). Retina vulnerable.

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23
Q

Colour Blindness

A

6% of population, X linked recessive
Protagonist: L (red) cone absent
Deuteranopia: M (green) cone absent
Deficits in blue cone are rare

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24
Q

Nyctalopia (night blindness)

A

Vitamin A deficiency - secondary to dec ingestion, defective absorption etc. Precursor of visual pigments. RODS are first affected, hence night blindness issues.

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25
Q

Retinitis Pigmentosa

A

Group of serious, predominantly genetically-determined degenerative diseases in which RODS preferentially degenerate
Early night blindness, followed by TUNNEL VISION, and total blindness
(Rods are in periphery, so if degenerating only central vision remains)

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26
Q

Cerebral Achromotopsia

A

Damage in Brodmann areas 18 and 37
See in shades of grey.
Hemiachromotopsia (one side lesion) is more common, but individual wouldn’t notice bc still have other eye and brain fills in.

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27
Q

Stereognosis

A

Identifying an object based on touch with eyes closed. If fails, could represent a parietal lesion.

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28
Q

Graphesthesia

A

Identify characters drawn on hand with eyes closed. If lost, could represent again a cortical lesion.

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29
Q

First Pain and Second Pain

A

First pain: sharp, carried by A delta fibres (1-6 microm, 4-36 m/s conduction velocity)
Second pain: dull, throbbing carried by unmyelinated C fibres (0.2-1.5 microm), 0.4-2 m/s conduction velocity)
Pseudounipolar

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30
Q

Substances released from damaged tissue that sensitize nociceptors

A

PG’s from damaged cells
Leukotrienes from damaged cells
Substance P from primary afferents

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31
Q

Descending Control

A

In addition to gate control, have descending control of pain.
Descending fibres with excitatory projections (5-HT or NE)onto enkephalinergic interneuron - releases enkephalin onto opioid receptors, blocking release of substance P dampening pain response.

Origins: PAG, Locus Coruleus (NE), Nucleus Raphe Magnus (5-HT)

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32
Q

Non Selective COX blockers

A

Aspirin, Ibuprofen

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33
Q

Selective COX (II)blockers

A

Celecoxib, Vioxx

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34
Q

Pain management surgical interventions

A

Ablative:
Cordotomy - restricted to cancer pain - ALS lesion, obliterate transmission along ALS
Dorsal root entry zone lesions - ie brachial plexus avulsion in motor vehicle accident, then lesion area of dorsal horn to prevent signal transmission

Stimulative:
Spinal cord stimulation - based on gate control, stim A beta fibres, might inhibit pain ie peripheral neuropathy
Deep brain stimulation of thalamus or PAG
Intraspinal medication - utilize the epidural space

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35
Q

Protanopia

A

No red cones. Causing confusions of red greens and yellows. Vision test looks green.

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36
Q

Deuteranopia

A

No green cones. Also a green vision test

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37
Q

Tritanopia

A

No blue cones. Picture looks red background with blue number.

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38
Q

Vestibular Schwannoma

A

Tumour of CN VIII. Hearing loss, tinnitus, equilibrium problems, vertigo. As tumour enlarges, can cause facial weakness (impinge VII root), numbness (onto V root), abnormal corneal reflex (V or VII roots.

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39
Q

Lesion of Abducens Root

A

Motor neurons in abducens activate ipsilateral lateral rectus.
Loss of voluntary lateral gaze in IPSILATERAL eye. DIPLOPIA
Looking straight - lesioned eye will deviate medially
Diplopia WORSE when looking TOWARD lesioned side in horizontal plane.

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40
Q

Caudal Basilar Pontine Lesion

A

Lesion could simultaneously damage exiting ABDUCENS fibres and CORTICOSPINAL axons. Alternating hemiplegia (paralysis)
Paralysis of lateral rectus IPSILATERAL to lesion (loss of voluntary lateral gaze toward affected side)
Paralysis of upper and lower extremities on opposite side of body.
Alternating, crossed deficits are characteristic of brainstem lesions.

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41
Q

Internuclear Opthalmoplegia (INO)

A

Lesion to MLF (medial longitudinal fasciculus)
Interrupts fibres ascending to motor nucleus of III.
IPSILATERAL LOSS of MEDIAL GAZE on side of lesion during attempted conjugate eye movements. R
Ie left INO indicates lesion of L MLF and L medial rectus
R INO indicates lesion of R MLF and R medial rectus

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42
Q

Lesion to abducens NUCLEUS

A

(Practically an abducens root lesion + INO)
IPSILATERAL LOSS of horizontal gaze IN DIRECTION OF LESION.
Affect alpha motor neurons going to lateral rectus on same side, and interneurons going toward alpha motor neurons of medial rectus on opposite side. Horizontal gaze to contralateral side is NORMAL

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43
Q

One and a half syndrome

A

UNILATERAL PONTINE LESION
Loss of medial and lateral voluntary movement IPSILATERAL to lesion (one)
Loss of MEDIAL horizontal mvmt CONTRALATERAL (half)

Abducens nucleus injury –> leads to the medial rectus prob contra and lateral rectus prob ipsilateral
MLF adjacent - conveying axons of abducens interneurons from opposite side fucks up the medial rectus of the ipsilateral side also

PARAMEDIAL PONTINE RETICULAR FORMATION/HORIZONTAL GAZE CENTER

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44
Q

Myasthenia Gravis (MG)

A

Autoantibodies blocking nAChR, or dmg postsynaptic.
Ocular movement disorders (diplopie, ptosis) initial deficits. Bc ACh is found in the motor neurons of CN nuclei
Movements of neck and tongue can be impaired, – dysphasia and dysarthria

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45
Q

Lesions in midbrain involving root of CN III and crus cerebri

A

Alternating hémiplégie. ipsilateral paral of most eye movement (ptosis, down and out, diplopia), and contralateral hémiplégie of extremities

46
Q

Damage to MLF (multiple sclerosis, or small vessel lesion)

A

Results in internuclear opthalmoplegia - on lateral gaze, OPPOSITE medial rectus will NOT adduct.

47
Q

CN deficits associated with diabetes mellitus, trauma, or pontine gliomas

A

VI dysfunction

Affected eye slightly ADDUCTED, DIPLOPIA pronounced on gaze TOWARD lesioned side.

48
Q

Damage in caudal and medial pons

A

May involve fibres of VI and adjacent CORTICOSPINAL Fibres in basilar pons
MIDDLE CROSSED HEMIPLEGIA.
IPSILATERAL paralysis of lateral rectus and CONTRA hémiplégie of extremities.

49
Q

Cerebral peduncle/weber syndrome

A

IPSILATERAL oculomotor paralysis
CONTRA sided hémiplégie of UE/LE
CONTRA paralysis of lower face

50
Q

RED NUCLEUS/CLAUDE SYNDROME

A

IPSILATERAL OCULOMOTOR paralysis
Contra loss of proprioception, discriminative touch, vibratory sense on UE
Contra hyperkinesia, CONTRA akinésie

51
Q

Lesion in Medial longitudinal fascicula

A

IPSILATERAL inter nuclear ophthalmoplegia

52
Q

Structures tested on visual pathway exams

A

CN II, optic chiasm, optic tract, LGN (thalamus), optic radiations (temporal and parietal lobes), visual cortex (occipital)

53
Q

Structures related to eye movements

A

Frontal eye field (frontal lobe), parietal-occipital eye field (parietal lobe), PPRF, CN VI (pons), CN III, IV, (midbrain), vestibular nuclei (medulla), MLF, floculonodular lobe (cerebellum)

54
Q

Corneal Reflex related structures tested

A

CN V, VN, VII, facial motor nuc (pons), spinal trigeminal nucleus (medulla)

55
Q

Pupillary light reflex structures tested

A

CN II, optic nerve, optic chiasm, optic tract; pretectal nucleus, EW nucleus (midbrain), CN III

56
Q

Bell’s Palsy

A

Idiopathic peripheral lesion of the facial nerve
Impairment of taste and hyperacusis often present (facial nerve innervates stapedius m, attenuating reflex, so deficient)
80-85% make full recovery within 3 months of onset.

Could result in total loss of corneal reflex action (blink) on affected side
Flattened nasolateral fold, unable to raise eyebrow and wrinkle forehead on affected side

57
Q

Otosclerosis

A

Conductive hearing loss example. Unknown cause
Abnormal formation of bone affecting stapes
1-2/100 in the UK (2:1 female to male)
Hearing loss, deafness if untreated, tinnitus
hearing aids, stapedotomy

58
Q

Presbyacusis

A

Age related hearing loss, progressive bilateral and symmetrical sensorineural hearing loss associated with aging, higher frequencies affected most

59
Q

Vestibular Schwannoma (example of sensorineural hearing loss)

A

Benign, usually slow growing tumour due to overproduction of Schwann cells, usually unilateral
Ipsilateral hearing loss, tinnitus, disturbance of balance (CN VIII)

Large tumour can occupy much of cerebellopontine angle (CPA) and can affect CN VII (ipsilateral facial weakness) and CN V (ipsilateral facial numbness)
CT scans enhanced with contrast, and MRI critical in early detection, helpful in microsurgical removal

(CN 5 comes out of pons but still passes through cerebellopontine junction, 578 pass through this junction)

60
Q

Menières Disease

A

Example of Sensorineural Hearing loss
Distortion of membranous labryinth from overaccumulation of endolymph –. 1. Fluctuating hearing loss 2. Occasional episodic vertigo 3. Tinnitus 4. Aural fullness
Physical distention leads to mechanical disturbance of organ of corti and otolithic organs

Diagnose by EXCLUSION
Oto-neuro exam, audiometry, MRI should be performed to EXCLUDE a tumour of CN VIII

61
Q

Cochlear Implants

A

Electrically stimulate the auditory nerve - reserved for profoundly deaf individuals. Externally microphone, speech processor, transmitter
internally: receiver and electrodes.
Allows for perception of sound but does NOT restore hearing

62
Q

Carotid Bodies

A

At carotid bifurcation. Sense pO2 (mainly), pCO2, and also pH. Send messages via glossopharyngeal (IX) to medulla

63
Q

Aortic bodies

A

At aortic arch. Sense pO2 and pCO2. Sense messages via vagus (CN X) to medulla.

64
Q

DRG Dorsal Respiratory Group

A

Forms caudal half of NTS. Primary target of visceral afferents carrying sensory info related to resp function, via CN IX and CN X.

65
Q

Cheyne Stokes respiration

A

Caused by lesions of corticospinal and corticobulbar fibres. Cortical damage, forebrain*. Respiration characterized by period of apnea, followed by waxing and waning of resp depth. May completely lose voluntary control of resp. Resp centres are intact but no longer under appropriate control.

66
Q

Apneustic breathing (inspiratory cramps)

A

Pontine lesions (PRG). Prolonged inspiratory plateaus of high lung volume followed by prolonged expiratory pauses with low lung volume. No longer have that off switch of inspiration. Long inspiration, hold it, then finally expire

67
Q

Ataxic breathing

A

Lower pons/ upper medullary lesions - randomly occurring large and small breaths alternating with prolonged periods of apnea. Damaged rhythmic centres, pre-botzinger, maybe botzinger as well

68
Q

Pneumotaxic Centre (Pontine Respiratory Group)

A

Essential for maintaining normal breathing pattern; inhibits apneustic centre. Switch off of inspiration
Signals ventral respiratory gropu - fine tunes breathing rhythm in sleep, speech, and exercise.

69
Q

Apneustic Centre

A

Lower pons. Tonic faciliation of inspiration by excitatory input to pre-botzinger complex.

70
Q

Dorsal Respiratory Group

A

Iputs from pulmonary stretch receptors, output is to respiratory motor neurons in the spinal cord.
Signals VRG. Integrates peripheral signals, receives visceral afferents

71
Q

Hyperventilation possible cause

A

Lesion in midbrain

72
Q

Stages of sleep and associated wave patterns

A 
Awake: alpha and b waves
1 nREM : theta waves
2 nREM: spindles and K complexes
3 nREM: delta waves (slow wave sleep)
4 nREM: Delta waves (slow wave sleep)
5 REM: Beta waves
73
Q

Components of the ARAS (Ascending Reticular Activating System)

A

PPT (pedunculopontine) and LDT (laterodorsal tegmental) ACh pons–> thalmus –> cortex
MAO ie raphe nuc (5HT), LC (NA), ventral teg (DA), tuberomammo (His) to cortex
Basal forebrain cholinergic to cortex (ACh, GABA)
Lateral hypothalamus (orexigenic)

74
Q

Fetal Exposure to Diethylstilbestrol (DES)

A

DES is a synthetic estrogen, was prescribed to reduce spontaneous abortion. Reported that prenatal exposure increased occurence of bisexuality and homosexuality in girls.
In rats, expereiments indicate DES exposure during critical period induces enlarged SDN in females (normally larger in males)

75
Q

Sexually dimorphic areas of the hypothalamus

A 
SDN (ie INAH 1 in humans)
INAH 2, 3, 4
Suprachiasmatic Nucleus 
Supraoptic nucleus
Paraventricular nucleus
Ventromedial nucles
76
Q

SDN

A

Significantly larger in males than females, and higher cell counts in males than females

77
Q

Hypothalamic nuclei in homosexual vs hetero

A

INAH-3 larger in hetero than home (2x as large)
INAH 3 also 2x as large in M as in F (hetero)
Correlated sexual orientation

78
Q

Suprachiasmatic Nucleus size differences m f

A

2x as large in males (possibly correlated with larger body size)

79
Q

Critical period for sexual differentiation

A

Prior to birth, 12-20 weeks gestation. result of testosterone secretion, peak in males during this time. NO comparable increase in either test or est in females during this time.
Testosterone is converted to estrogen via aromatase, and it is estrogen which exerts the effects on transmitter release and gene expresion. Cytoplasmic estradiol receptor protein, then enters ucleus.

80
Q

Brain region that synthesizes GnRH

A

Arcuate Nucleus of hypothalamus

81
Q

Sertoli Cells

A

Secrete anti-mullerian hormone (AMH), lose mullerian duct and maintain wolffian duct.

82
Q

Androgen Insensitivity Syndrome

A

Mutation in PG-21 receptors/androgen receptors. Prevents androgen binding to receptor or receptor binding to DNA response elements.
NO ovaries, but appear female. (testosterone has no effect). Amenorrhea, no pubic hair, breast growth, shallow vag.

83
Q

Symptoms of Upper motor neuron lesion

A

Loss of voluntary control
Hyperreflexia & Spasticity
Extensor plantar response (babinski)
First flaccid paralysis, later spastic paralysis
Slow onset disuse muscle atrophy (very slow)
Clonus

84
Q

Lower motor neuron lesion

A 
Symptoms occur ipsilateral
Hyporeflexia/areflexia
Flaccid paralysis
Rapid onset muscle atrophy
Fasciculations and fibrillations
85
Q

Projections to Primary motor cortex

A

Primary somatosensory, Basal ganglia (via thalamus and premotor), cerebellum (via thalamus), premotor cortex, posterior parietal cortex (BA 5, 7)

86
Q

Projections to premotor cortex that then project to Primary motor cortex

A

Cerebellum and basal ganglia (both via thalamus), posterior parietal (BA 5,7), and primary somatosensory

87
Q

Consequences of an internal capsule infarct

A

Masticatory muscles are OK (bilateral)
CONTRA paralysis of lower facial muscles
Deviation of tongue CONTRA to lesion(away)
Hoarsness, dysphagia, dysarthria, deviation of uvula TOWARD lesion ipsi~
Inability to shrug shoulder on same side, inability to turn head to contralateral side (accessory nucleus)

88
Q

Ventromedial (anteromedial ) spinal motor tracts incl

A

Lateral vestibulospinal, medial vestibulospinal, pontine (medial) reticulospinal

89
Q

Lateral spinal motor tracts incl

A

Lateral corticospinal, rubrospinal, medullary reticulospinal

90
Q

Two types of LMNs

A

Alpha LMN: innervates extrafusal muscle fibres, contraction, movement
Gamma LMN: inn intrafusal muscle fibres within muscle spindles, contraction, regulation via sensory afferents. Feedback from muscle spindle afferents.

91
Q

ALS Lou Gehrigs

A

Degeneration of UMNs and LMNs (anterior horn of spinal cord and of CN V, VII, X, and XII)
onuf;s nucleus not affected - urinary and fecal continence mostly preserved
Atrophy, weakness, fasciculations, cramping (
Loss of bulk in thenar, hypothenar, inteorssei, arm, shoulder
Reduced cough reflex - risk of aspiration pneumonia
Crnail motor nuclei - difficulty coughing and speaking. Tongue weakesss, atrophy, fasciuculation.
Death from respiratory aspiration pneumonia.

92
Q

Anterior Spinal Artery Syndrome

A

Damage to LMN (ventral horn) and UMN (lateral corticospinal tracts) and ALS
Spastic paraparesis, BILATeral babinski, bilateral loss of P and T, retention of urine, sexual functions impaired

93
Q

Central medullary syndrome (most commonly syringomyelia)

A

Cyst along central canal usually expands ventrally and compresses ventral horns (LMNs) and ventral white commissure (ALS). Could expand to corticospinal? Segmental muscular atrophy, loss of Pain and Temperature starting 2 levels below in a dermatomal fashion.
May produce pain and weakness, and stiffness in the back, shoulders, arms, legs. Disturb sweating, sexual function, and bladder & bowel control

94
Q

Function of lateral hypothalamus orexigenic projctions

A

Facilitate the MAO projections and enhance ARAS

95
Q

Function of ARAS during nREM sleep

A

ARAS is actively inhibited by projections from GABAergic ventrolateral pre-optic nuclei (VLPO)
Cholinergic and monoaminergic systemss are SLOWED down in NREM sleep.

96
Q

ARAS

A

ON during wakefulness and REM sleep

97
Q

VLPO in sleep

A

GABAergic projections inhibit ARAS during nREM sleep

98
Q

REM sleep

A

PPT (pedunculopontine) and LDT (laterodorsal tegmental) cholinergic projectinos to the pontine reticular formation, to thalmus are ON.
Motor system is inhibited (except oculomotor and respiratory muscles)
Illogical, bizarre dreams perhaps due to lack of prefrontal cortex activity.

99
Q

Kluver-Bucy Syndrome

A

Removal of anterior parts of temporal lobe including amygdala, parts of hippocampal formation - dramatic change in emotional behaviour.
Emotional flattening, inappropriate mounting, oral fixations.
Loss of fear, hyperphagia, PSYCHIC BLINDNESS
memory impariment, utilization behaviours,, seizures

100
Q

Le Doux’s theory

A

High road versus low road - low road bypasses cortex, goes straight from thaalmus to amygdala - fast emotional response to threat
LGN - SC - amygdala-

101
Q

Some causes of Kluver-Bucy syndrome in humans

A

Bilateral glioma, head trama, status epilepticus, herpes simplex encephalitis, post-epilepsy surgery

102
Q

Urbach Wiethe Disorder

A

Bilateral Amygdala calcifications

No fear response to emotional faces, aversive stimuli, or life threatening events.

103
Q

Fear Acquisition (classical conditioning)

A

Simultaneous inputs from conditioned stimulus (ie auditory sound) and from somatosensory (shock), simultaneously route to the BASOLATERAL amygdala, which projects to the central nucleus of the amygdala. Central nucleus then projects to Central grey (freezing), Lateral hypothalamus (SNS), and BNST (HPA axis)

104
Q

Formation of Extinction memory

A

Simultaneous input from conditioned stimulus (ie auditory), and normal somatosensory input project to ventromedial Prefrontal cortex (VMPFC), which projects to amygdala, down-regulating amygdala firing.

105
Q

Role of hippocampus in contextual memory

A

Hippocampus tracks context, and either up-regulates amygdala firing in threatening situations, or down-regulates firing in safe context.

106
Q

Lesion to orbitofrontal cortex

A

Patient maintains negative expectancies in absence of genuine threat.

107
Q

Damage to ventromedial PFC

A

Patient cannot form a new fear extinction memory, sponteaneous recovery of fear after extinction

108
Q

Hippocampal injury regarding fear

A

Fear response generalizes to safe environments, or new unconditinoed stimulus with similar features. Poor differentiation of save versus threatening stimuli and contexts

109
Q

Temporal lobe epilepsy

A

Aura (deja vu, sense of fear, olfac. or gust sensations, epigastric sens)
Behavioural automatisms (lip-smacking, automatic mvmts.)
Mood changes (anxiety, depression)
Attention/cognitive co-morbidities
Ictal amnesia
Depression highly correlated - 17% get MDD compared to 10% of general pop. Much higher chances even if recurring TLE

110
Q

Midbrain lesions breathing pattern

A

Hyperventilation. Rapid, low amplitude constant breathing

111
Q

Bilateral damage to medulla breathing pattern

A

Respiratory arrest

Neuro (6 decks)

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