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Module 4 - Neuro > 2 - Pathology > Flashcards

2 - Pathology Flashcards

1
Q

What is Benign Paroxysmal Positional Vertigo?

A

-Vertigo: from the patient’s perspective, the false sensation that the world is moving
-BPPV: episodic vertigo typically coming on suddenly after moving head (turning over in bed, looking up, etc)
-due to otoconia from macule falling into semicircular canals
-cause excitation of the crista ampullaris without proper stimuli
-canal can be determined by the direction of the nystagmus/perceived spinning
-~90% are Posterior Canals -> fast phase = UP and Rotated
Tx: Dix Hallpike Maneuver; Epley Maneuver

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2
Q

What is vestibular neuritis? What tests are used for VN?

A

-NV w/o hearing loss: caused by neuroptopic viruses in the vestibular nerve; causes persistent (if not continuous) vertigo
-NV w/ hearing loss: Meniere’s Disease (episodic vertigo) and viral labyrinthitis (persistent vertigo)
** patient perceives to be spinning TOWARD bad ear (room
spinning away from bad ear)
Tests:
1) Covered Fundus Exam: since fixation can overcome nystagmus, covered eye fundus exam removes the fixation and can expose nystagmus (fundus nystagmus is opposite of globe)
2) Head Thrust Exam: tests the VOR; eyes drift to the DAMAGED side
3) Fukuda Step Test: patient marches in place with eyes closed; patient drifts TOWARDS damaged ear
4) Alexander’s Law: in unilateral vestibular lesion, nystagmus is more intense when looking in the Fast direction
TX:
1) Meclizine: antihistimine-> mild
2) Phenergan/Compazine: anti-emetic w/ anti-cholinergic -> strong
3) BZ’s

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3
Q

What are some tx for motion sickness?

A

1) Scopolamine
2) Promethazine (Phenergan)
3) Meclizine (Antivert)
4) Dimenhydrinate (Dramamine)
5) Diphenhydramine (Benedryl)
Other: ginger, peppermint oil, isopropyl alcohol vapors

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4
Q

What is the mechanism of hearing damage following sound exposure?

A

1) >150dB -> middle ear damage
2) damage restricted to inner ear
3) >110dB -> damage to organ of corti (outer hair cells most sensitive)
4) when inner hair cells die, neurons slowly disappear
5) when they survive, stereocilia can be damaged
6) at low thresholds, without cell/hair damage, nerve terminal swelling can cause hearing loss

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5
Q

What is the presentation of damage to the following cranial nerves:

1) Occulomotor
2) Trochlear
3) Abducens

A

1) Occulomotor damage: pupil points down and abducted due to unopposed action of the lateral rectus and the superior oblique; also will have ptosis
2) Trochlear damage: pupil tends to extort due to unopposed action of the interior oblique; most pronounced when looking down to the unaffected side -> will tend to compensate by tilting head to affected side, forcing the good eye to intort and relieve diplopia
3) Abducens damage: pupil tends to adduct due to unopposed action of the medial rectus; tend to compensate by turning head to bring the affected eye into focus

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6
Q

Describe the mechanism of accomadation.

A

1) accommodation increases the refractive power of the lens by making it thicker and thus allows the eye to focus on a closer object
2) to thicken the lens the ciliary muscles are contracted via parasympathetic innervation, this brings the zonular fibers closer to the lens body and relieves their tension
3) the lens then “relaxes” into a thicker form; most of the change occurs in the anterior direction which brings the lens closer to the cornea and increases the power
4) can increase the diopter of the lens from 20 to ~34
5) during accommodation the pupils also constrict (miosis) to sharpen the image

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7
Q

Describe myopia.

A

Myopia -> Nearsightedness

1) the lens is focused in front of the retina -> the eyeball is too long
2) concave lenses used for correction since it causes some divergence of the rays and lengthens its path

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8
Q

Describe hyperopia.

A

Hyperopia -> Farsightedness

1) image is focused behind the retina -> eyeball is too short
2) convex lenses are used to increase the power of the eye to focus the image closer/on the retina (+ diopters)
3) Presbyopia -> age related decreased elasticity of the lens produces farsightedness since the eye cannot accommodate for closer objects

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8
Q

Describe astigmatism.

A

1) refractive error due to asymmetric curvature of the cornea
2) results in inability to focus image at any distance
3) requires cylindrical lens to compensate for the irregularities of the cornea

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9
Q

Describe the following agnosias:

1) Simultanagnosia
2) Akinetopsia
3) Prosopagnosia
4) Achromatopsia

A

M-Pathway
1) Simultanagnosia: inability to perceive two objects simulaneously; trouble seeing multiple objects as a whole -> typically a bilateral lesions in the superior parietal cortex
2) Akinetopsia: inability to see moving objects; life is a strobe light
P-Pathway
3) Prosopagnosia: inability to recognize a face; can see/identify other objects, but can’t associate the face with a particular person -> typically a bilateral lesion to the Inferior Temporal Cortex
4) Achromatopsia(Color Blind): inability to see colors even though there are functional cones; if a unilateral lesion to the P-Pathway/ITC, the contralateral hemifield is seen in black and white, while the other half is normal color; depth perception and spatial reasoning is preserved

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10
Q

Describe the presentation of a unilateral lesion to the following locations:

1) abducens nerve
2) abducens nucleus
3) MLF
4) trochlear nerve
5) occulomotor nerve

A

1) abducens nerve: loss of lateral rectus -> failure of eye to abduct and eye will “drift” center due to unopposed medial rectus, but no impact on adduction and convergence
2) abducens nucleus(right): loss of lateral rectus and conjugate mvmt of medial rectus -> both eyes deviate left in forward position or right gaze, left gaze and convergence still ok
3) MLF (left): left eye drifts left, when right gaze left eye stays center and the right eye will abduct but then start right nystagmus
4) trochlear nerve: loss of superior orbital -> eye drifts up, extorts and adducts, most pronounced looking medially when the affected eye fails to depress
5) occulomotor nerve: complete ptosis and unopposed action of superior orbital and lateral rectus -> eye is dilated and fixed in the depressed, abducted position

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11
Q

Describe the following cerebellar lesions:

1) Vestibulocerebellum (nodulus)
2) Spinocerebellum (vermis)
3) Hemispheric

A

1) Vestibulocerebellum/Nodulus: common in children w/ medulloblastoma presents as ataxic gait, head tremor, and nystagmus
- relieved by recumbent position as it relives the trunk muscles from compensating for gravity
2) Spinocerebellum/Vermis: typical of alcohol degeneration and classically presents with truncal/unsteady gait
- NOT relieved by lying down since the defect is in the coordination/planning of walking mvmts
3) Hemispheric: caused due to numerous causes and present as ipsilateral asynergia
- dysmetria (distance of mvmts), intention tremor, dysdiadochokiesis (trouble with rapid repeated mvmts), gait ataxia, decomposition

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12
Q

Describe the clinical presentation of trigeminal neuralgia (Tic Douloureux).

A
  • patient experiences recurrent, brief (~15 min) episodes of intense pain in the CN V distribution, typically V2/3
  • cause is unknown, but may be due to anomalous blood vessels compressing the nerve along its path
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13
Q

Describe the types and presentations of facial nerve palsy.

A

1)Peripheral Facial Nerve Palsy: by convention this includes any lesion on the nerve, in the motor nucleus of the VII in the lower pons and the ventral lower pons where the motor fibers exit the brainstem (even though 2 of them are in the CNS)
-Ipsilateral facial paralysis -> results from lesion of the nerve prior to division
- depending on where in its course, hyperacusis, impaired taste, impaired salivary activity, impaired lacrimation (dry eye) can occur
2) Bell’s Palsy: most common facial nerve disorder; causes degredation of all branches of the facial nerve from an unknown cause
-typically takes hours-days, and occurs unilaterally
-function MAY return gradually over 2-3 weeks, but ~20% don’t recover
3) Voluntary Central (UMN) Facial Palsy: involves damage to the UMN tract for CN VII which is the Corticobular Tract that travels from the primary motor cortex to the Facial Motor Nucleus
-input from the Corticobulbar Tract is bilateral for motor neurons to the Upper face, but unilateral/contralateral for motor neurons to the Lower face
-therefore, a unilateral lesion to the tract will cause lower face paralysis, since upper face can still be stimulated by the ipsilateral side
-frequently, Corneal Reflex and emotionally motivated facial expressions are preserved
-

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14
Q

Describe the mechanism of the Pupillary Light Reflex.

A

1) light stimulates the photoreceptors in the eye which causes stimulation of the ganglion cell whose axons projects via the optic nerve to the inpsilateral and contralateral pretectal nuclei (splitting at the chiasm)
2) Neuron 2 projects from the pretectal nuclei bilaterally to the Edinger-Westphal Nuclei (OMC)
3) E-W gives rise to Neuron 3, which is a preganglionic parasympathetic nerve that travels ipsilaterally to the ciliary ganglion via CN III
4) from the ciliary ganglion, Neuron 4 (ciliary nerve) penetrates the schlera to innervate the sphincter puppilae and constrict the iris
5) this causes bilateral constriction when one eye is stimulated with light

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15
Q

Describe the mechanism of the Corneal Reflex.

A

1) sensation from the cornea is carried by the long ciliary nerves of the opthalmic nerve (V1)
2) the cell bodies(psuedounipolar) for the long ciliary nerve are in the trigeminal ganglion in the floor of the medial cranial fossa
3) from the ciliary ganglion the neuron axon travels to the spinal V nuclues
4) another neuron then projects bilaterally to the Facial Motor Nuclei
5) this stimulates a motor fiber in CN VII which travels to the eye too orbicularis oculi, palpebral part to cause blinking

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16
Q

What is Benedikt’s Syndrome?

A

Benedikt’s = Tegmental Syndrome

1) it is a lesion of the midbrain that affects the Red Nucleus, Superior Cerebellar Peduncle, Medial Lemniscus, STT, CN III tract
2) Red N. and SCP: contralateral cerebellar signs -> intention tremor, ataxia
3) Med Lemniscus and STT: loss of contralateral 2-pt touch, vibration, proprioception, pain and temp
4) CN III tract: ipsilateral oculomotor palsy-> ptosis, depressed and abducted eye, dilated w/o pupillary reflex, loss of accomodation

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17
Q

What is Weber’s Syndrome?

A

Weber’s Syndrome = Superior Alternating Hemiphegia

1) injury to the ventral mesencephalon at the midbrain level causes damage to the Corticospinal, Corticobulbar and Oculomotor Tracts
2) CST -> contralateral hemiparesis
3) Corticobulbar -> contralateral hemiparesis of the LOWER face (upper face is innervated bilaterally)
4) CN III -> ipsilateral Oculomotor Palsy (ptosis, dilated, depressed/abducted, no pupillary reflex or accomadation)

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18
Q

What is Middle Alternating Hemiplegia?

A

Middle Alternating Hemiphegia

1) injury to the ventral mesencephalon at the lower pons level causes damage to the Corticospinal, Corticobulbar and AbducensTracts
2) CST -> contralateral hemiparesis
3) Corticobulbar -> contralateral hemiparesis of the LOWER face (upper face is innervated bilaterally)
4) CN VI -> ipsilateral paralysis of Lateral Rectus causing medial deviation and diplopia (no nystagmus)

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19
Q

What is Millard-Gubler Syndrome?

A

Millard-Gulbar Syndrome

1) injury to the ventral upper lateral pons level causes damage to the Corticospinal, Corticobulbar and Abducens and Facial Nerves
2) CST -> contralateral hemiparesis
3) Corticobulbar -> contralateral hemiparesis of the LOWER face (upper face is innervated bilaterally)
4) CN VI -> ipsilateral paralysis of Lateral Rectus (medial deviation w/o nystagmus)
5) CN VII -> ipsilateral paralysis of entire face (LMN)

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20
Q

What is Inferior Alternating Hemiplegia?

A

Inferior Alternating Hemiplegia

1) injury to the ventral medulla level causes damage to the Corticospinal tract and Hypoglossal Nerves
2) CST -> contralateral hemiparesis
2) CN XII -> ipsilateral tongue weakness causing deviation TOWARD the affected side

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21
Q

Define the following terms:

1) Bradykinesia
2) Hypokinesia
3) Akinesia
4) Resting tremor
5) Dystonia
6) Athetosis
7) Chorea
8) Ballismus
9) Tics

A

Hypokinetic Movement DO
1) Bradykinesia: slow, labored movements
2) Hypokinesia: few movements
3) Akinesia: no movements
Hyperkinetic Movement DO
4) Resting tremor: rythmic, oscillating movements that disappear during purposeful movement
5) Dystonia: sustained contraction of body part(s) that result in abnormal, distorted forms of the face, trunk or limbs
6) Athetosis: slow, twisting, writhing movements that flow from one body part to another
7) Chorea (the dance): nearly continuous, non-purposeful movements that are fluid or jerky
8) Ballismus: flinging movements of the proximal limb muscles
9) Tics: quick repetetive movemtents made after an urge to do so, with relief following -> often in face or neck, but can be verbal

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22
Q

Describe the presentation of Parkinson’s Disease.

A

1) idiopathic degenerative disease causing loss of domapinergic neurons in SNc
2) results is less dopamine in striatum, which leads to less stimulation of the Direct Pathway => suppression of movement
3) Hypokinetic Model: bradykinesia, rigidity, postural instability
4) Resting Tremor is seen, but it is not well explained by the hypokinetic model

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23
Q

Describe the clinical presentation of Huntington’s Disease.

A

1) hereditary neurodegenerative disease thought to be associated w/ CAG repeats; leads to progressive degeneration of Spiny (GABA/Enkephalin) Neurons
2) loss of these Enkephalin Neurons leads to less indirect pathway stimulation, therefore facilitative movement
3) Hyperkinetic Model: chorea, hyptonia
4) also causes dementia and behavioral/personality changes

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24
Q

Describe the clinical presentation of Ballism/Hemiballism.

A

1) typically due to vascular injury to the Subthalamic Nucleus
2) causes less indirect pathway excitation => facilitating movement
3) Hyperkinetic model: characteristic is ballismus- wild flinging of the limbs from the proximal muscles
4) unilateral lesions cause hemiballism, while bilateral results in ballism

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25
Q

Describe the clinical presentation of Kallmann Syndrome.

A

1) clinical association between lack of “sense of smell” and reproductive function
2) higher in males
3) genetic disorder which leads to low levels of Testosterone, LH, FSH

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26
Q

What is Karsakoff Syndrome?

A
  • syndrome characterized by memory loss
  • chronic alcoholism leads to thiamine deficiency which causes particular insult to mammillary bodies and anterior and dorsal medial thalamic nuclei
  • this significantly interrupts the Papez Circuit and presents as memory loss, confusion and confabulation
27
Q

Describe the clinical presentations to lesions in the following areas:

1) planum temporale
2) Wernicke’s area
3) Brocha’s area
4) Superior Longitudinal Fasciculus

A

1) planum temporale is within Wernicke’s area and if impaired on the dominant side is thought to cause dyslexia
2) Wernicke’s area: auditory association cortex on dominant side participates in language comprehension; Wernicke’s Aphasia is characterized by sensory, fluent, receptive aphasia -> form word-like sounds that make no sense
3) Brocha’s area: pars opercularis and pars triangularis of the dominant hemisphere; Brocha’s Aphasia characterized by inability to produce language, thought comprehension is unaffected
- lesion to the non-dominant side is associated w/ monotonic speech, since it is thought this location is responsible for intonation
4) Superior Longitudinal Fasciculus (Arcuate): interconnects Wernicke’s and Brocha’s area; lesions to this area are characterized by inability to repeat words or phrases; typically comprehension and original production is unimpaired, but cannot repeat when directed

28
Q

What is apraxia?

A

-inability to carry out a learned sequence of movements due to a cerebral cortex lesion (i.e. toothbrushing, hammer, etc)

29
Q

Describe astereognosis.

A

-inability to recognize an object my feeling it

30
Q

What is contralateral neglect?

A
  • patient is unaware of the contralateral hemisphere(typically left)
  • due to large lesion to the right parietal cortex
31
Q

Describe Blepharitis.

A

1) inflammation of the eyelid margin (external)
2) itching, redness and thickening; can also lose eye lashes
3) though there are many causes, most common is Staph Aureus
Tx: typically can just use conservative -> lid scrubs, warm compresses and let heal on its own
-then progress to topical and then oral antibiotics

32
Q

Describe Conjunctivitis.

A

Pink eye

1) inflammation of the conjunctiva
2) presents as eye redness, pain, burning/gritty sand in eye, sticky discharge/crust in the mornings
3) MANY causes:
- Bacterial: Staph Aureus, Strep Pneum, H. Influenzae -> Topical Antibiotics
- >typically presents as unilateral infection, PURULENT discharge that clears when wiped away, more edema than virus, not associated with enlarged node, and is continuous all day
- Viral:l ADENO, Herpes simplex, measles, varicella -> topical lubrication for eye
- > typically presents as bilateral, CLEAR discharge, wiping eye produces profuse tearing, little edema, preauricular node enlarged, discharge worst in the AM

33
Q

Describe Infectious Keratitis.

A

1) presents as red eye w/ sensation of a foreign body, photophobia, trouble keeping eye open, CORNEAL OPACITY
2) stains well w/ flouresceine stain
3) MANY causes
- Bacteria: Staph Aureaus, Pseudomonas, Cornybacteria, Chlamydia
- Virus: Adeno, HSV1
- Fungal: Fusarium
- Protozoa: Acanthamoebae

34
Q

Describe Trachoma.

A

1) Infectious Keratitis caused by Chlamydia trachomatis
2) recurrent infections of the palpebral conjunctiva causes scaring
3) can progress to contraction of the eyelid and eyelashes turning inward, which then cause additional damage to the eye(corneal opacification, keratitis, and blindness)
4) leading cause of infectious BLINDNESS
5) Tx w/ antibiotics

35
Q

Describe Endophthalmitis.

A

1) inflammation of the vitreous or aqueous humor
2) presents as decreasing vision, eye ache, hazy view of the retina, but fever is uncommon
3) can cause Hypopyon: layering of WBC in anterior chamber which is seen on exam as a white accumulation on the bottom of the iris
4) Acute: staph aureus, staph epidermis, strep’s
Subacute: aspergillus (uncommon)
Chronic: proprioibacterium acnes
5) seen as Complication of Cataract surgery, post-trauma, hematogenous spread(IE, UTI, GI,etc)

36
Q

Describe Otitis Media.

A

1) infection of the inner ear, typically associated with the spread of an infection of an URI
2) nasal infection/congestion leads to blocking of the Eustachian tube causes secretions of the middle ear to build up and promote growth of the pathogen
3) typically presents as ear pain, hearing loss, vertigo, ear discharge (if perforated), fever (in children)
4) exam of the tympanic membrane: red, swollen, immobile and opaque
5) Bacteria: Step pneumoniae, H. Influenza, Psudomonas
- Virus: RSV, Rhino, Influenza, Adeno
6) Tx: viral typically resolves on its own, so no tx is givin initially; once thought to be bacterial, give Abx

37
Q

Describe Sinusitis.

A

1) infection of the paranasal sinuses, typically via swelling and blockage of a drainage path which causes fluid build up in the sinus
2) presents as nasal congestion, nasal discharge, maxillary TOOTH pain, facial pain, facial pressure, tenderness over sinuses, decreased transillumination
3) Acute: Viruses (Rhino, Influ, Parainfluenza, Adeno); Bacterial (Strep pneumonia, H. Influenza, Strep pyrogen, Staph aureus
->Tx: due to difficulty of differentiating viral from bacterial, and the preponderance of viral cases; recommend withholding Abx for 7-10d and just give NSAIDs, decongestant, topical steroids
4) Chronic: Bacteria (same); Fungal (Aspergillis, Mucormycosis, molds)
5) fungal infections in immunocompromised patients can cause gross bony destruction
3)

38
Q

What is Delirium?

A
  • Definition: Neuropsychiatric syndrome reflecting disturbed CNS function due to an underlying medical condition
  • Criteria: 1) disturbance of consciousness w/ reduced ability to focus, sustain or shift attention
    2) change in cognition or perception not due to dementia
    3) acute onset -> hours to days
    4) indication that is caused by the direct physiological consequences of a GMC
39
Q

Describe the clinical presentation of delirium.

A

1) presence of underlying GMC
2) acute onset -> hours to days
3) disturbance in consciousness: spectrum from clouding to coma; attention difficulties
4) disturbance in cognition: changes in orientation, general confusion, delusions (usually simple and transient), perceptual disturbances (distortions, hallucinations, illusions)
- auditory less common, visual most common; other senses strongly suggestive of organic cause of illusion/hallucination
5) short term memory deficit
6) can alter sleep-wake cycle
7) psychomotor disturbances: hyper or hypoactive; tremors; lack of coordination
8) affect lability
9) WAX and WANE in 24 hrs (common)

40
Q

What is the pathophysiology of delirium?

A

1) initial, precipitating injury initiates a cascade of metabolic and neurochemical events that result in impaired function
2) excess Dopamine; diminished ACh -> overexcited, uninhibited
3) Dopamine causes psychotic symptoms, ACh causes confusion, cognitive deficits
4) inflammatory cytokines released causing neuron death, alteration of BBB and glial cell function
5) overall results in physiologic stress -> hypoxia, BBB damage, HPA axis dysregulation, decreased Thyroid action

41
Q

What are the common etiologies of delirium:

1) urgent
2) broader

A 
Urgent -> WHHHMPS
1) Wernicke's encephalopathy
2) Hypoxia 
3) Hypoglycemia
4) Hypertensive encephalopathy
5) Meningitis/Encephalitis
6) Poisoning
7) Stroke
Broader = I WATCH DEATH
1) Infection
2) Withdrawal
3) Trauma
4) CNS path
5) Hypoxia
6) Deficiencies (B12/folate/niacin/thiamine)
7) Endocrinopathies 
8) Acute Vascular
9) Toxins/Drugs
10) Heavy Metals
42
Q

Differentiate the following dx:

1) delirium
2) dementia
3) depression
4) schizophrenia

A

1) Delirium: acute onset impaired consciousness, inattention, and memory; Wax and Wane over 24hrs; hallucinations can be anything, but tactile, gustatory and olfactory strongly suggest organic cause; delusions are transient and inconsistent
2) Dementia: insidious, progressive decline of memory; consciousness and attention frequently preserved until late stages; hallucinations are visual or auditory; delusions are paranoid, often fixed
3) Depression: variable time course; consciousness and memory are intact, but attention is impaired and auditory hallucinations are common; delusions are variable with mood
4) Schizophrenia: variable time course; consciouness and memory are preserved, but attnetion is imparied; auditory hallucinations are most common; delusions are complex and persistent

43
Q

What are typical EEG readings from in delirium?

A

1) Diffuse slowing: most common; associated w/ ACh toxicity, TBI, hepatic encephalopathy, hypoxia
2) Low-Voltage Fast Activity: typical of demetia tremens; EtOH withdrawal, BZ toxicity
3) Spikes/polyspikes: nonconvulsive ictal pattern
4) Left/bilateral slowing or delta waves: acute confusional migraine; usually in adolescents
5) Epileptiform activity: status w/ prolonged confusional state; nonconvulsive status and complex partial status epilepticus

44
Q

What are the tx options for delirium?

A

1) tx the underlying etiology!
2) supportive therapy: SPOCCC
- Support
- Protect
- Orient
- Calm
- Communicate
- Comfort
3) Antipsychotics: Haldol; Atypicals(rispiredone, olanzapine, quetiapine)
4) Benzodiazepine: used ONLY for EtOH and GABA-ergic withdrawal

45
Q

Define Dementia.

A

Definition: impairment of memory and other cognitive functions w/o alteration of consciousness
Criteria: memory problems + one or more of the following: aphasia, apraxia (complex motor), agnosia (naming), or executive functioning

46
Q

Describe Alzheimer’s Disease.

A

1) most common form of dementia; >65 = late onset; plaques
3) ApoE clears B-amyloid, but ApoE4 (Ch 19) is less efficient
4) build up of B-amyloid plaques leads to inflammation and neuronal death
5) Tau protein (from neuronal cytoskeleton) also becomes twisted and tangled also leading to cell death
6) Tx to slow progress: mild-moderate = ACEi (Donezepil); moderate-severe = NMDA antagonists (memantine)
7) supportive therapies/tx are very important in this population and with regard to their caregivers

47
Q

Describe Vascular Dementia.

A

1) 3 subtypes: Multi-infarct, Microvascular, Critical Area Infarct
2) Multi-infarct: step-wise decline due to repeated cortical/subcortical strokes
3) Microvascular: thickening of the subcortical arteriole walls; slowing of cognition and increased depression
4) Critical Area: single infarct in important area causing cognitive deficits
5) Tx: control risk factors (HPTN, smoking, DM, hyperlipidemia); ACEi (Donezepil)

48
Q

Describe Lewy Body Dementia.

A

1) third most common dementia; due to Lewy bodies deposit in brain causing dysfunction
2) characterized by memory loss + parkisonian movement disorders
3) vivid hallucinations are also common
4) symptoms vary significantly from day to day; wax and wane can make it look like delirium
5) VERY sensitive to antipsychotics and can be a fatal reaction

49
Q

Describe the following dementias:

1) Frontotemporal/Picks
2) Huntington’s
3) Creutzfeldt-Jabob
4) HIV-dementia

A

1) Frontotemporal: Behavior changes (disinhibition) and Language difficulties; early onset w/ ~30% genetic; Pick’s is the same except there are Pick’s Bodies (tau positive)
2) Huntington’s: autosomal dominant mutation on Ch 4(CAG repeat reduced); associated with Choreiform movements, early onset (35-50) and high rates of suicide/psychiatic symptoms
3) Creutzfeldt-Jacob: prion disease (inherited, infectious or sporadic), presents 50-70, characterisitcally Triphasic complexes on EEG and myoclonus on exam; universally fatal
4) HIV: low CD4 and high viral load; presents as apathy, psychomotor retardation and inattention, but preserved language; tx w/ HART which can cure the dementia

50
Q

Describe amnesia.

A

1) inability to learn new information
2) many causes
3) Chronic Alcoholism can lead to thiamine deficiency:
- Wernicke’s encephalopathy: ataxia, opthalmoplegia, delirium
- Korsakoff’s syndome: dense anteriograde amnesia
4) Tx w/ IM Thiamine before a glucose load leads to infarct

51
Q

Describe the clinical presentation of a migraine.

A

1) POUND:
- Pulsatile
- One-day (4-72hrs)
- Unilateral
- Nausea/vomiting
- Disabling intensity
2) photophobic, worsened by EtOh,
3) frequently ~monthly around mentral cycle or some stressor
4) strong family connection

52
Q

Describe TBI.

A

1) traumatically induced physiologic disruption of brain function
2) Acute indications: Loss/Alteration of consciousness, Post-Traumatic Amnesia, skull fracture
3) Symptoms: headaches, dizziness, fatigue, balance

53
Q

Delineate Mild, Moderate and Severe TBI.

A
  • ranking based on Glasgow Coma Scale, Alteration of Consciousness, Loss of Consciousness or Post-Traumatic Amnesia
    1) Mild: GCS (13-15), AOC(24), LOC (>30min, 24hrs, 24), LOC (>24), PTA (>7d)
54
Q

What are the types of tissue damage common in TBI?

A

1) Diffuse Axonal Injury: shearing/stretching of axons causes disruption of brain signaling (static); presents as generalized deficits (confusion, poor attention, slow processing, memory)
2) Contusions: brain bruise; Coup-contusion on same side as injury; Counter-Coup-contusion on opposite side; causes deficits specific to the location of the bruise
3) Penetrating Injury: focal injury based on location; cause intracranial bleeding and infection
4) Secondary/Delayed: slow to present; intracranial bleeds, increased ICP, blood loss, excitotoxicity

55
Q

Describe the course of post-concussive symptoms in the following areas:

1) symptoms
2) cognition
3) emotional
4) functional

A

1) symptoms: highly variable; Mild = typically resolve in days-wks; Mod/Severe = fewer initial symptoms, but resolve slower
2) cognition: Mild = subtle problems in processing speed, memory and attention; Mod/Severe = highly variable based on location; severe deficits following a mild concussion strongly suggests another etiology
3) emotional: Mild = exacerbated emotional problems; Mod/Severe = depression, apathy, disinhibition, substance abuse
4) functional: Mild = avoid driving/dangerous tasks until symptoms fully resolve; Mod/Severe = highly variable; rely on rehab team, but should re-engage slowly

56
Q

Define the types of seizures.

A

Partial: localized onset
1) Simple Partial: sensory “auras” or limited, unilateral motor convulsions; No loss/alteration of consciousness; 20-60sec
2) Complex Partial: still localized sensory/motor phenomenon, but consciousness is compromised; post-ictal confusion and lethargy; Most Common refractory type in adults; 30s-2min
3) Partial secondarily generalized: begins as a local/partial seizure but develops into a generalized tonic-clonic; 1-2min
Complex: no localized onset
4) Grand Mal (tonic-clonic): loss of consciousness; tonic spasms followed by jerking clonic convulsions; prolonged post-ictal stupor; 1-2min
5) Absence (Petite Mal): abrupt interruption of consciousness; automatisms are common, or mild jerking; NO post-ictal effects, which helps distinguish it from Complex Partial; ~30s

57
Q

Describe

1) Status Epilecpticus
2) Infantile spasms
3) Febrile seizures

A

1) SE: continuous and prolonged seizure (5-10min) or multiple seizures in rapid succession; most common is tonic-clonic which is life threatening; requires CV, respiratory and metabolic management
2) Infantile Spasms: epilectic seizure characterized by myoclonic spasms; first attack before 1yr; refractory to most antiseizures
3) Febrile Seizures: NOT epilepsy; brought on by high fever in infants/small children

58
Q

Describe nasal polyps.

A

Nasal Polyps

  • chronic inflammation leads to development of mucosal polyps
  • polyps are endematous mucosa w/ cystic mucousal glands and inflammatory infiltrate of neuts, eosinophils, and plasma cells
  • presents as nasal congestion, rhinorrhea, or headaches
  • more common in >20y/o, but very rare in if present in children, should be screened for CF
59
Q

Describe Macular Degeneration.

A

Macular Degeneration

  • thickening of the Bruch membrane leads to damage of the retinal vasculature and photoreceptors
  • presents as progressive vision loss, metamorphopsia, and central/paracentral scotomas
  • Dry = vision loss, no vasculature damage -> no Tx
  • Wet = damage to retinal vasculature leading to exudates and hemorrhages, eventually develops into scar (YELLOW appearance) -> prior to scar, give VEGF inhibitors or oblate the new vessels with photocoagulation
60
Q

Describe the effect of Diabetes Mellitus on the eye.

A

1) diabetes results in damage to lens, iris and thickening of the basement membrane
2) Background (preproliferative) retinopathy: thickening of the basement membrane of the retinal vasculature leads to formation of aneurisms and macular edema
3) This can lead to non-perfusion, which will induce increased VEGF to be released
4) the VEGF will promote neovascularization
5) Proliferative Retinopathy: new vessels that sprout from existing vessels on the surface of either the optic disc or the surface of the retina
6) this neovascularization can lead to hemorrhage or detachment of the vitrous, retina or RPE -> retinal tearing
7) neovascularization in the iris can also lead to damage that resembles glaucoma

61
Q

Describe MS.

A
  • autoimmune disease that results in the degradation of myelin in the CNS, while preserving the axons
  • this produces sharply defined plaques in white matter, frequently at the angles/edges of ventricles
  • also characteristically shows perivascular, monocytic inflammation
  • symptoms are due to a series of acute, focal lesions that vary in time and location
62
Q

Describe ALS.

A

Amyotrophic Lateral Sclerosis

  • motor denervation disease of unknown cause
  • results in upper and lower motor neuron death, principally of the pyramidal motor system (voluntary movement of body and face)
  • extraoccular and sphincter muscles are usually preserved, along with other neuro functions -> they “become trapped within their own body”
  • fasciculations of the body and the tongue are characteristic of the disease
63
Q

Describe Alzheimer’s.

A

Alzheimer’s disease

  • neurodegerative disease characterized by deposition of A-B amyloid; presence of tau/ubiquitin tangles; and amyloid angiopathy
  • formation of B-amyloid is associated with errors in Ch. 1, 14, 19, 21, and 22
  • presents as insidious memory loss, bx changes, and mood instability and progresses to Aphasia, Apraxia, Amnesia, Agnosia
  • diffuse atrophy is also characteristic, with the most pronouced in the frontal, temporal and partietal lobes -> results in enlarging of ventricles (hydrocephalus ex vacuo)
  • plaques tend to develop in the Hippocampus, amygdala and neocortex
64
Q

Describe Polio virus.

A

Polio virus

  • enterovirus that can (1%) cause an infection of motor neurons in spinal cord and brainstem
  • presents as progressive, flaccid paralysis/LMN signs
  • 1% of those w/ CNS disease develop paralysis or death (respiratory failure)
  • hemorrhage, congestion and edema is common in spinal cord/brainstem
  • Vaccine has largely controlled infection in developed world (Salk = killed, Sabin = live)
65
Q

Describe Cysticercossus.

A

Cysticercossus

  • when the larvae of a tapeworm are ingested, they are absorbed by the gut and form cysts, which can be distributed throughout the body
  • the cyst can induce an inflammatory response, which can cause seizures
  • after the cyst has been destroyed, form a scar and then a calcified lesion, which can also induce an immune response and seizures
  • most common after eating meat (pork) in countries w/ poor food controls
66
Q

Describe Rabies.

A

Rabies

  • RNA virus carried by animal saliva (bats/dogs most common) that infact the PNS, travel to the dorsal root ganglia and infect the CNS
  • once the DRG is infected, prodromal symptoms begin = neuropathic pain at bite site
  • once CNS is infected, a “furious encephalitis” begins and results in phobic spasms and autonomic dysfunction, and then paralysis and death
  • Gross: degeneration, inflammation of brainstem and basal ganglia
  • Micro: NEGRI BODIES = eosinophilic cytoplasmic inclusions which are oval or bullet shaped

Module 4 - Neuro (11 decks)

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