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Brain & Behavior Extras > Midterm Pathologies > Flashcards

Midterm Pathologies Flashcards

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1
Q

Anencephaly

A

Clinical Presentation: absence of brain and skull; elevated AFP in amniotic fluid and maternal blood; frog-like appearance of fetus; polyhydramnios
MOA: cranial end of the neural tube fails to close leading to no forebrain and calvaria
*associated with maternal T1DM
*folate will decrease risk

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2
Q

Spina Bifida

A

Clinical Presentation: elevated AFP; occulta: dimple or patch of hair over the vertebral defect; meningocele: protrusion of meninges; meningomyelocele: protrusion of meninges and spinal cord
MOA: caudal neuropore fails to close, but neural tissue continues to develop normally; closed neural tube necessary to induce formation of vertebral arches

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3
Q

Craniosynostosis

A

Clinical Presentation: scaphocephaly or oxycephaly/turricephaly
MOA: premature closure of sagittal, lambdoid, and coronal sutures leading to deformities of the head which inhibit proper brain development
*scaphocephaly = early closure of sagittal suture
*oxycephaly or turricephaly = early closure of coronal suture

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4
Q

Amyotrophic Lateral Sclerosis (ALS)

A

Clinical Presentation:
lower signs - flaccid paralysis with muscle atrophy, fasciculations, weakness with decresed muscle tone, impaired reflexes, negative Babinski sign
upper signs - spastic paralysis with hyperreflexia, increased muscle tone, positive Babinski sign
MOA: degeneration of upper and lower motor neurons of the corticospinal tract; anterior motor horn degeneration leads to lower motor neuron signs; lateral corticospinal tract degeneration leads to upper motor neuron signs
*SOD1 mutation present in some familial cases (leads to free radical injury in neurons)
*atrophy and weakness of hands is early sign

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5
Q

Corticospinal lesions

A

Clinical Presentation: weakness or paralysis on the contralateral side of the body
MOA: rostral to decussation at pyramids - lesions to upper motor neuron in pyramidal tract, brainstem, or forebrain
Clinical Presentation: weakness of paralysis on the ipsilateral side of the body
MOA: caudal to decussation at pyramids - lesions to lateral corticospinal tract, ventral horn, ventral root of the spinal cord, or peripheral alpha motor neuron.

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6
Q

DC/ML Lesions

A

Clinical Presentation: Sensory (vibration, proprioception, discriminative touch) deficits on the contralateral side of the body
MOA: rostral to decussation at Dorsal Column Nucleus lesions to medial lemniscus, thalamus, thalamic radiation, or forebrain
Clinical Presentation: Sensory (vibration, proprioception, discriminative touch) deficits on the ipsilateral side of the body
MOA: caudal to decussation at Dorsal Column Nucleus - lesions to gracile/cuneate fasciculi, dorsal root, and peripheral nerve

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7
Q

AL Lesions

A

Clinical Presentation: Sensory (pain and temperature) deficits on the contralateral side of the body
MOA: Rostral to decussation at anterior white commissure - lesions to spinothalamic/Lissauer’s tract, thalamus VPL, thalamic radiation, or forebrain
Clinical Presentation: Sensory (pain and temperature) deficits on the ipsilateral side of the body
MOA: Caudal to decussation at anterior white commissure - lesions to substantia gelatinosa in dorsal horn, dorsal root, and peripheral nerve

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8
Q

Epidural Hematoma

A

Clinical Presentation: cranial nerve III palsy
MOA: Collection of arterial blood between dura and the skull; classically due to fracture of the temporal bone with rupture of middle meningeal artery
*lens shaped (biconvex) lesion of CT; not crossing suture lines
*herniation is a lethal complication

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9
Q

Subdural Hematoma

A

Clinical Presentation: progressive neurologic signs; increased occurrence in elderly due to age-related cerebral atrophy
MOA: Venous blood pooling underneath dura and covers the surface of the brain. Due to tearing of bridging veins that lie underneath the dura and arachnoid usually because of trauma
*crescent-shaped lesion of CT that crosses suture lines
*herniation is a lethal complication

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10
Q

Subarachnoid hemorrhage

A

Clinical Presentation: sudden SEVERE headache. produces blood in the CSF; causes severe headache, stiff neck, loss of consciousness
MOA: typically due to rupture of an aneurysm as arteries pass within the subarachnoid space

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11
Q

Tentorial Hernia

A

Increase in intracranial pressure above the tentorium cerebelli (i.e. epi or subdural hematoma) or decreased pressure below (i.e. CSF leak) brain may herniate through tentorial incisure

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12
Q

Scalping

A

hair is caught in piece of machinery - hair, skin, connective tissue, and epicranial aponeurosis pulled away as a unit; skull with its periosteal connective tissue layer is left exposed.

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13
Q

Whiplash

A

Clinical Presentation: anterior longitudinal ligament or anterior neck muscles are stretched and/or torn; may rupture intervertebral discs, break posterior arch of atlas or dens of axis
MOA: hyperextension (or flexion) of neck due to sudden forward acceleration of the body

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14
Q

Hangman Fracture

A

Breakage of the posterior arch of the axis with atlas, odontoid process, and body of C2 staying with the head; rest of the vertebral column breaks inferiorly.

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15
Q

Huntington Disease

A

Clinical Presentation: chorea that can progress to dementia and depression; aggression; average age of presentation is 40 y.o.
MOA: degeneration of the GABA neurons in the caudate nucleus of basal ganglia; AD inheritance (expanded CAG trinucleotide repeats in the Huntington gene)
*SSRI or ampakine treatment increases BDNF production in patients
*inheritance shows anticipation; suicide is common cause of death

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16
Q

Peripheral Neuropathy

A

Clinical Presentation: affects sensation, movement, gland, and organ function
MOA: damage or disease affecting peripheral nerves due to diabetes, metabolic disorder, traumatic injury, etc.

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17
Q

Bell’s Palsy

A

Clinical Presentation: Ipsilateral paralysis of upper and lower muscles of facial expression
MOA: Idiopathic cause of facial nerve palsy
Tx: corticosteroids, acyclovir; most pts have gradual recovery of function

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18
Q

Facial Nerve Palsy

A

Clinical Presentation: Ipsilateral paralysis of upper and lower muscles of facial expression
MOA: Peripheral CN VII/Facial (LMN) lesion
Tx: corticosteroids, acyclovir; most pts have gradual recovery of function
*can be caused by Lyme disease, HSV, Herpes Zoster, Sarcoidosis, and tumors

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19
Q

Cutting of Facial Nerve

A

Clinical Presentation: Paralysis of single or group of muscles of facial expression
MOA: Deep facial lacerations may cut branches of the facial nerve
Tx: laceration medial to lateral canthus of the eye then cut branches will re-innervate their target muscles and fx will be restored over time

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20
Q

Congenital Insensitivity to Pain with Anhidrosis (CIPA)

A

Clinical Presentation: devoid of all pain and thermal sensations but with normal touch, vibration, and proprioception; variable degrees of mental retardation, learning deficits, and emotional distrubances
MOA: Loss of function mutation of NTRK1 that results in developmental apoptosis of a specific neuronal population; loss of NGF-dependent primary sensory neurons and postganglionic SYMP neurons
*Lissauer’s and Spinothalamic tracts can’t be distinguished at autopsy
Tx: management of Sx and prevention of injury and infection; removal of baby teeth in young pts
*most pts don’t live past 3 y.o. due to hyperthermia

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21
Q

Arachnoid Granulations

A

hypertrophy of the arachnoid villi results in arachnoid granulations which may form pits on the inner table of cranial bones along the superior sagittal sinus

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22
Q

Brown-Sequard Syndrome

A

Clinical Presentation: Ipsilateral UMN signs and loss of tactile, vibration, and proprioception sense and contralateral pain/temp loss below the level of the lesion; ipsilateral sensation loss and LMN signs at level of lesion
MOA: hemi-section of the spinal cord

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23
Q

Acute Inflammatory Demyelinating Polyraduculopathy (Guillian-Barre syndrome)

A

Clinical Presentation: symmetric ascending muscle weakness/paralysis starting in the lower extremities; autonomic dysregulation; 2/3 have antecedent flu illness; peak in 60y.o.
MOA: autoimmune destruction of Schwann cells causing inflammation and demyelination of peripheral nerves and motor fibers
Tx: supportive care, IVIG, and plasmapharesis
*assc with infections
*increased CSF protein with normal cell count
*almost all pts survive and most recover completely in weeks to months

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24
Q

Charcot-Marie-Tooth Disease

A

Clinical Presentation: lower extremity weakness, sensory deficits, wasting, decreased reflexes pes cavus, hammertoe; onset usually by 20 y.o,
MOA: hereditary nerve disorder related to defective production of protein involved in structure and function of peripheral nerves or myelin sheath; due to segmental duplication of PMP22 gene (70% of cases)
Histo: large onion bulbs; hypertrophy of neurons
*usually AD inheritance; associated with foot deformaties

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25
Q

Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP)

A

Clinical Presentation: proximal and distal weakness, sensory change, hyporeflexia over 2 months or more; may be progressive or relapsing/remitting
MOA: autoimmune destruction of Schwann cells causing inflammation and demyelination of peripheral nerves and motor fibers
Histo: lymphocyte infiltrate of the nerve itself, thinly myelinated axons, macrophages, onion bulbs
Tx: corticosteroids, IVIG, plasma exchange

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26
Q

Lepromatous Leprosy

A

Clinical Presentation: symmetric polyneuropathy with loss of pain; generalized fatigue, numbness of ears, forehead, toes, and fingers.
MOA: Schwann cells infected by M. Leprae (a mycobacterium)
Histo: demyelination and remyelination

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27
Q

Diptheria

A

Clinical Presentation: weakness and paresthesias

MOA: Exotoxin infection causing demyelination

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28
Q

Varicella-Zoster Virus infection

A

Latent virus travels to sensory nerves of the skin causing sensory ganglia neuronal degeneration and axonal degeneration

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29
Q

Glioblastoma Multiforme (GBM)

A

Clinical Presentation: nausea, vomiting, headache
MOA: malignant tumor of astrocytes usually in the cerebral hemisphere and crosses corpus callosum
Histo: Regions of necrosis surrounded by tumor cells and endothelial cell proliferation; tumor cells GFAP positive; vascular proliferation
*most common malignant CNS tumor in adults; poor prognosis

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30
Q

Meningioma

A

Clinical Presentation: seen more in women; presents as seizures
MOA: benign tumor of arachnoid cells; often near surfaces of brain and parasaggital region
CT/MRI: round mass attached to the dura
Histo: Whirled pattern, psammoma bodies may be present; progesterone receptors frequent
Tx: resection and/or radiosurgery
*most common adult benign CNS tumor; rare in children

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31
Q

Hemangioblastoma

A

Clinical Presentation: Can cause secondary polycythemia (b/c makes EPO)
MOA: most often cerebellar, brain stem, or spinal; associated with VHL syndrome
Histo: closely arranged thin-walled capillaries, minimal intervening parenchyma; often rich in lipids
Tx: surgery
*benign slow growing tumor

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32
Q

Schwannoma

A

MOA: benign tumor of Schwann cells; involves cranial or spinal nerves most commonly cranial VIII (abducens); compresses nerve but doesn’t infiltrate
*NF2 association
Histo: encapsulated, verocay bodies, hyalinized blood vessels; tumor cells are S-100 positive
Tx: resection or steriotactic radiosurgery

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33
Q

Oligodendroglioma

A

Clinical Presentation: may present with seizures
MOA: malignant tumor of oligodendrocytes usually involving frontal lobe
CT/MRI: calcified tumor in white matter; fried-egg appearance of cells, chicken wire capillary pattern; calcifications, perinuclear halos
*relatively rage, slow growing; IDH-1 mutation frequent

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34
Q

Pituitary Adenoma

A

Clinical Presentation: bitemporal hemianopia due to pressure on optic chiasm; hypo or hyperpituitarism
MOA: hyperplasia or single type of cell in the pituitary; most often prolactinoma

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35
Q

Pilocytic Astrocytoma

A

MOA: benign astrocyte tumor often in cerebellum, 3rd ventricle, and optic nerves
Histo: cystic lesion with mural nodule; Rosenthal fibers and eosinophilic granular bodies; GFAP positive tumor cells

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36
Q

Medulloblastoma

A

Clinical Presentation: usually arises in small children; can compress 4th ventricle and cause non-communicating hydrocephalus
MOA: malignant tumor derived from granular cells of the cerebellum
Histo: small, round, blue cells; rosettes may be present
Tx: surgery, adjuvant therapy
*poor prognosis; tumor grows rapidly and spreads via CSF

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37
Q

Ganglioglioma

A

Clinical Presentation: found in temporal lobe of children/YA with early onset epilepsy
MOA: glioneuronal neoplasm with dysplastic ganglion cells and neoplastic glial cells
Histo: cystic; well differentiated
Genetics: BRAF of V600E mutation
*good prognosis

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38
Q

Ependymoma

A

Clinical Presentation: hydrocephalus; usually in children
MOA: Ependymal cells, malignant; most commonly in the 4th ventricle
Histo: perivascular pseudo-rosettes and acellular regions, ependymal canals
Tx: surgery and radiation
*poorer prognosis for children

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39
Q

Meningeal Carcinomatosis

A

MOA: malignant tumor cells found in the subarachnoid space, often from small cells carcinomas or adenocarcinomas (esp breast and lung)
*can’t resect = bad prognosis

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40
Q

Central Neurocytoma

A

Clinical Presentation: seen in young adults
MOA: tumor found intraventricularly usually attached to the septum pellucidum in region of foramen of Monro
Histo: neuronal cells
*favorable prognosis

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41
Q

Pleomorphic Xanthoastrocytoma

A

Histo: large, bizarre cells; chronic inflammation, eosinophilic granular bodies, mural nodule with a cyst
Tx: surgery
*better prognosis than diffuse astrocytomas

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42
Q

Lymphoma

A

Clinical Presentation: 2-3% of all brain tumors; single or multiple lesions
MOA: Diffuse large B-cell lymphoma of the CNS; associated with immune deficiency
Tx: surgery (steriotactic biopsy), steroids (avoid pre-op), radiation, chemo
*MRI is most sensitive technique to detect

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43
Q

Atypical Teratoid Rhabdoid Tumor (ATRT)

A

Clinical Presentation: Found in young children (<5y.o.); found in posterior fossa or supratentorial location
MOA: high frequency of SMARCB1 inactivation
Histo: rhabdoid cells that are polyphenotypic
*poor prognosis

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44
Q

Myxopapillary Ependymoma

A

MOA: form of ependymoma
Histo: little blue ependymal cells, degenerative changes, pink hyalinized blood vessels, mucin
*slow growing, low grade tumor with good prognosis

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45
Q

Neurofibroma

A

Clinical Presentation: can be cutaneous
MOA: tumor that arises most commonly on solitary nerve section
Histo: low cellularity, fibroblasts and Schwann cells, lots of collagen
Tx: have to remove the nerve when you resect the tumor

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46
Q

Malignant Peripheral Neve Sheath Tumor (MPNST)

A

MOA: can arise de novo or from a plexiform neurofibroma
Histo: very cellular, large ugly nuclei with prominent, mitotic figures, necrosis

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47
Q

Myoclonus/ Clonus

A

sudden, brief, uncontrolled muscle contraction

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48
Q

Hypotonia/Hyporeflexia

A

diminished deep tendon reflexes; flaccid muscle
MOA: early stage spinal cord transection (2-3) weeks where alpha motoneuron excitability is diminished; following peripheral nerve or ventral horn injury (LMN/alphaMN)

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49
Q

Hypertonia/Hyperreflexia

A

heightened deep tendon reflexes, muscle rigidity (spasticity, clonus)
MOA: upper motor neuron lesion

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50
Q

Rigidity

A

sustained muscle contraction at rest (in the absence of any voluntary movement)

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51
Q

Spasticity

A

little of no contraction at rest

MOA: late phase of spinal cord transection; corticospinal lesions

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52
Q

Open angle glaucoma

A

Clinical Presentation: painless; elevated IOP, progressive peripheral visual field loss.
MOA: primary cause is unclear; associated with age, AA race, family history; secondary causes: blocked trabecular meshwork from WBCs, RBCs, retinal elements
Histo: optic disc atrophy; thinning of outer rim of optic nerve head
Tx: pharmacological or surgical lowering of IOP

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53
Q

Closed/narrow angle glaucoma

A

Clinical Presentation: Elevated IOP, progressive peripheral visual field loss. conjunctival infection, fixed mid-dilated pupil. “steamy” or edematous cornea.
MOA: enlargement or forward movement of lens against the central iris obstructing normal aqueous flow through pupil and peripheral iris gets pushed against cornea
Histo/Radiology: optic disc atrophy; thinning of outer rim of optic nerve head
Tx: IV Diamox, laser iridotomy, topical glaucoma medications

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54
Q

Conjunctivitis

A

Clinical Presentation: red eye; allergic = itchy, viral = watery discharge, bacterial = grittiness, irritation, mucopurulent discharge
MOA: inflammation of the conjuctiva from virus, bacterial, or allergic reaction

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55
Q

Papilledema

A

MOA: optic disc swelling due to increased ICP from excessive CSF; blood, esp venous blood, pools in the veins on the surface or the retina
*enlarged blind spot and elevated optic disc with blurred margins

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56
Q

Sty (hordeolum)

A

Clinical Symptoms:
Internal sty - inflammation of meibomian/tarsal gland just under conjunctival side of the eyelid
External sty - inflammation of eyelash follicle or lid-margin glands
MOA: acute purulent inflammation of the eyelid, generally caused by staph aureus

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57
Q

Chalazion

A

Clinical Symptoms: normally not infected or painful
MOA: lump in the eyelid as a result of the chronic blockage of one of the meiboinan/tarsal glands
Tx; hot compresses 4x daily or lancing the inner surface of the eyelid

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58
Q

Exopthalmos

A

Clinical Presentation: eyes that protrude slightly; seen in patients with Grave’s disease
MOA: increased size of the extraocular muscles and edema in the orbit due to autoimmune rxn to TSH receptor antigen which is expressed in retroorbital tissues including extraoccular muscles

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59
Q

Strabismus

A

Clinical Presentation: 2-3% of the population (more common in Caucasians and females)
MOA: pathological misalignment of the visual axis that cause a loss of depth perception and binocular vision

60
Q

Esotropia

A

one or both eyes turn inward; more common form of strabismus
*form of strabismus

61
Q

Exotropia

A

one eye deviates outward; rare

*form of strabismus

62
Q

Presbyopia

A

trouble seeing up close

MOA: with increased age, lens becomes less elastic and can’t round up as much when ciliary muscle contracts

63
Q

Venous Nicking

A

during HTN the arteries become swollen and tend to restrict venous return as arteries cross the veins of the fundus

64
Q

CN IV Damage

A

(trochlear)

eye moves up (especially with contralateral gaze), head tilt toward unaffected side

65
Q

CN VI Damage (Abducens Nerve Palsy)

A

Clinical Presentation: double vision in which two images appear side by side
MOA: medially directed eye that can’t abduct (turn outward): often due to conditions that increase intracranial pressure and stretch abducens nerve

66
Q

CN VII Damage

A

MOA: damage to zygomatic/temporal branch of facial nerve (CN VII) leads to dysfunction of orbicularis oculi muscle so can’t close eyes properly
Tx: place gold weights in the upper lid to aid closing to protect the cornea from drying

67
Q

Von Hippel-Lindau Disease

A

Clinical Presentation: hemangioblastomas in the retina, brain stem, cerebellum, spine; angiomatosis, bilateral renal cell carcinoma, pheochromocytomas
MOA: AD inheritance, inactivation of the VHL tumor suppressor gene

68
Q

NF2 (Neurofibromatosis Type 2)

A

Clinical Presentation: bilateral acoustic schwannomas, multiple meningiomas, gliomas, hamartomas
MOA: autosomal dominant; mutation in the protein merlin

69
Q

Dislocated Jaw

A

Clinical Presentation: pain locking of the jaw
MOA: dislocation of temporomandibular joint; occurs when mouth is opened too wide or when mouth is bumped when open, head of mandible slides too far anteriorly over the articular tubercle, locking the jaw open
Tx: place was of material on the occlusal surface of teeth while applying downward pressure with fingers placed in the vestibule of the oral cavity

70
Q

Mandibular Tori

A

Clinical Presentation: 90% bilaterally; more common in Asian and Inuit populations
MOA: benign bony protrusions form the medial wall of the mandible towards the oral cavity

71
Q

Tooth Cavity

A

acids released form bacteria erode through the enamel into the sodter dentine

72
Q

Root Canal

A

cavity extends to the pulp of the tooth

*pulp material is removed, destroying the internal blood supply and innervation and packed with antibiotics, then sealed

73
Q

Uvular Deviation

A

Clinical Presentation: uvula is not midline
MOA: can indicate a lower motor neuron lesion of CN X which innervates most of the muscles of the soft palate
*uvula will deviate away from the affected side

74
Q

Uvulitis

A

Clinical Presentation: uvula is the most inflamed structure in the posterior pharynx of a febrile patient
MOA: inflammation of the uvula often from infection (group A strep most common)

75
Q

Bifid Uvula

A

Clinical Presentation: mildest form of cleft palate

MOA: associated with Loeys-Dietz syndrome, an AD genetic condition similar to Ehlers-Danlos and Marfans

76
Q

Torticollis

A

Clinical Presentation: holding head tilted to one side; difficulty turning the head
MOA: tearing of the sternocleidomastoid muscle during passage through the birth canal - muscle shortens in response to being torn

77
Q

Spasmodic Torticollis

A

*rare, sudden contraction of the sternocleidomastoid muscle

78
Q

Hiccups

A

diaphragmatic spasm which causes sudden inhalation of air which interrupted by reflex closure of the glottis

79
Q

Laryngeal Cancer

A

25% of head and neck cancers
MOA: vocal cords are area of transition from on epithelial type to another, so they are susceptible to cancer
*95% arise from squamous epithelial cells

80
Q

Epiglottitis

A

Clinical Presentation: can have excessive swelling which can interfere with breathing
MOA: inflammation of the epiglottis; often due to strep pneumonia or staph aureus
Tx: hospitalization, IV antibiotics, intubation

81
Q

Laryngitis

A

inflammation of vocal cords due to viral infection (usually) of respiratory epithelium within the larynx; can also be due to acid reflux
*true vocal cords turn from white to red and thicken due to edema; increased mass of vocal cord limiting their vibration

82
Q

Superior Laryngeal Nerve Damage

A

Clinical Presentation: weak, rough, easily fatiguing voice; can’t sing high pitches
MOA: unilateral paralysis of cricothyroid muscle
*touch supraglottic mucosa to see if causes cough reflex to test this nerve function

83
Q

Vocal Cord Paralysis

A

loss of innervation (recurrent laryngeal from vagus: CNX) to laryngeal muscles causes passive closure of the glottis
Tx: intubation

84
Q

C6 Radiculopathy

A

decreased bicep, triceps, and brachioradialis reflex; weakness of biceps, triceps, and flexor carpi radialis. Numbness in first two fingers

85
Q

C7 Radiculopathy

A

hand numbness and weakness just of the middle finger, weakness of triceps and decreased triceps tendon reflex

86
Q

Radial Neuropathy

A

weakness of arm affecting elbow, wrist, and finger extension

87
Q

Median Neuropathy

A

decreased radial flexion of hand, flexion of distal phalanx and digits 2/3, abduction of thumb

88
Q

Ulnar Neuropathy

A

decreased abduction of digits 2-5; decreased ulnar flexion of hand and of distal phalanx 4/5

89
Q

L4 Radiculopathy

A

weak knee extension and ankle dorsiflexion

90
Q

S1 Radiculopathy

A

weakness of plantar flexion, tow flexion, to extension, and foot eversion

91
Q

Femoral Neuropathy

A

decreased sensation to lateral thigh, episodic burning and numbness to lateral thigh

92
Q

Peroneal (Fibular) Neuropathy

A

weakness of ankle dorsiflexion, ankle eversion, and toe extensors

93
Q

Cryptogenic Sensory Polyneuropathy (CSPN)

A

Type of distal symmetric peripheral neuropathy
Clinical Presentation: “stocking and glove” sensory loss
MOA: chronic distal symmetric neuropathy. selective vulnerability of the longest neurons
Tx: symptom control

94
Q

Diabetic Peripheral Neuropathy

A

Type of distal symmetric peripheral neuropathy
Clinical Presentation: “stocking and glove” sensory loss
MOA: elevated fasting blood sugar leads to NEG of neurons and neuropathy. selective vulnerability of the longest neurons
Tx: symptom control

95
Q

Thyroglossal Duct Cyst

A

Clinical Presentation: midline masses below the hyoid bone. May interfere with swallowing.
MOA: thyroid tissue that did not fully migrate out of the thyroglossal duct. Generally runs posterior to the hyoid bone
Tx: surgery
*common in children 2-10y.o,

96
Q

Holoprosencephaly

A

Clinical Presentation: moderate - cleft lip/palate; severe - cyclopia
MOA: failure of the left and right hemispheres of the brain to separate; may be related to SHH pathway mutation
*can be seen in Patau syndrome and fetal alcohol syndrome

97
Q

Fetal Alcohol Syndrome

A

Clinical Presentation: craniofacial defects
MOA: alcohol causes apoptosis of pre-migratory neural crest cells during the first month of development when midline structures are established

98
Q

Treacher Collins Syndrome (TCS)

A

Clinical Presentation: maral hypoplasia (underdevelopment of zygomatic bones); underdeveloped mandible, malformed or missing ears, down-slanting palpebral fissures
MOA: Autosomal dominant inheritance; due to not enough neural crest cells proliferating and migrating to branchial arches.

99
Q

Pierre Robin Sequence (PRS)

A

Clinical Presentation: micrognathia of mandible, cleft palate, glossoptosis (posteriorly placed tongue)
MOA: defect in neural crest cell affecting mandible development; environmental and genetic factors.

100
Q

DiGeorge anomaly

A

Clinical Presentation: CATCH-22: cardiac outflow tract anomalies, abnormal facies, thymic aplasia, cleft palate, hypoparathyroidism
MOA: deletion of the long arm of chromosome 22 (22q11) causing errors in the development of the branchial arches (3 and 4)

101
Q

Global Cerebral Ischemia

A

Clinical Presentation: mild - transient confusion; severe - diffuse necrosis, vegetative state
MOA: global ischemia to the brain - low perfusion, acute decrease in blood flow, chronic hypoxia, repeated hypoglycemia

102
Q

Ischemic Stroke

A

Thrombotic - rupture of atherosclerotic plaque, often at a branch point
Embolic - thromboemboli (often from left side of the heart blocking the MCA); hemorrhagic infarct at periphery of cortex
Lacunar - secondary to hyaline arteriosclerosis; involves lenticulostriate vessels causing small cystic infarcts

103
Q

Intracerebral hemorrhage

A

Clinical Presentation: severe headache, nausea, vomiting, eventual coma
MOA: bleeding into the brain parenchyma (due to rupture of Charcot-Bouchard microaneurysm of lenticulostriate vessels)
*HTN complication; most common at basal ganglia

104
Q

Multiple Sclerosis

A

Clinical Presentation: neuro deficits with periods of remission; blurred vision in one eye, vertigo, scanning speech, hemiparesis; internuclear opthalmoplegia; lower extremity loss of sensation or weakness
MOA: autoimmune destruction of CNS myelin and oligodendrocytes; associated with HLA-DR2
MRI: periventricular plaques (areas of white matter de-myelination);
Lumbar Puncture: increased lymphocytes, increased Ig and MBP (myelin basic protein)
Tx: high dose steroids for acute attacks, interferon beta for long term- slows progression of Dz

105
Q

Parkinson Disease

A

Clinical Presentation: TRAP - Tremor at rest, Rigidity in extremities, Akinesia/bradykinesia, Postural instability and shuffling gait
MOA: loss of dopaminergic neurons in the substantia nigra of the basal ganglia; related to aging; unknown etiology
Histo: loss of pigmented neurons in substantia nigra and round eosinphilic inclusions of alpha-synuclein (Lewy bodies)

106
Q

Acoustic Neuroma

A

Clinical Presentation: disrupted vestibular and acoustic function; affected movement of muscles of facial expression taste and salivary gland secretion and anterior 2/3 of tongue
MOA: Schwann cell tumor of the vestibular nerve; can also affect function of the facial cranial nerve
*Associated with NF-2

107
Q

Facial Nerve Upper Motor Neuron Lesion

A

Clinical Presentation: contralateral paralysis of lower muscles of facial expression - forehead spared (frontalis)
MOA: destruction of the motor cortex or connection between motor cortex and facial nucleus in pons

108
Q

Facial Nerve Lower Motor Neuron Lesion

A

Clinical Presentation: Ipsilater paralysis of the upper and lower muscles of facial expression, hyperacusis, loss of taste sensation to anterior 2/3 of tongue
MOA: destruction of facial nucleus of CN VII

109
Q

Trigeminal Neuralgia

A

Clinical Presentation: sudden, severe pain in the regions covered by the trigeminal nerve
MOA: generally due to aberrant (redundant) cerebral arteries that compress the foot of the trigeminal nerve; most often only affects one of the branches. Causes focal area of demyelination with “cross talk” between bare axons
Tx: carbamezapine

110
Q

Vagus Nerve Lesions

A

Clinical Presentation: unilateral - hoarseness; difficulties swallowing; uvula deviates to the unaffected side
MOA: lesions causes loss of function of the intrinsic muscles of the larynx; inability to elevate the soft palate and contract the pharynx muscles necessary for swallowing

111
Q

CN XII LMN Lesion

A

Clinical Presentation: Tongue deviation to the same side as the lesion
MOA: lesions causes loss of function of the muscles of the tongue (except palatoglossus)

112
Q

Cataracts

A

Clinical Presentation: painless, often bilateral opacification of the lens often decreasing vision
MOA: congenital (galactosemia, galactokinase deficiency, trisomies, Marfan, Alport) and acquired (age, smoking, alcohol, excessive sunlight, DM, trauma) risk factors

113
Q

Uveitis

A

Clinical Presentation: may have hypopyon (leukocytic exudate and anterior chamber) or conjunctival redness
MOA: inflammation of uveal tract (iris + choroid + ciliary body)

114
Q

Age-related Macular Degeneration

A

Clinical Presentation:
Dry - deposition of yellowish extracellular material in and between Bruch’s membrane and retinal pigment epithelium
Tx: multivitamin and antioxidant supplements
Wet - rapid loss of vision due to bleeding secondary to choroidal neovascularization
Tx: anti-VEGF injections
MOA: degeneration of macula causing distortion and loss of central vision

115
Q

Diabetic Retinopathy

A

Clinical Presentation: Retinal damage
MOA:
Non-proliferative - damaged capillaries leak blood; fluids and lipids seep into retina causing hemorrhages and macular edema
Fundoscopic: cotton wool spots, venous nicking, intraretinal microvascular abnormalities
Proliferative - chronic hypoxia results in new blood vessels forming with resultant traction of retina
Fundoscopic: neovascularization of iris and disc; vitreous hemorrhage

116
Q

Retinal Detachment

A

Clinical Presentation: visual loss
MOA: separation of neurosensory layer of the retina from the outermost pigmented epithelium leading to degeneration of photoreceptors
Fundoscopic: crinkling of retinal tissue and changes in vessel direction
*more common in pts with high myopia and history of head trauma
*surgical emergency

117
Q

Retinitis

A

MOA: retinal edema and necrosis often due to virus (can be bacterial or parasitic)
*may be associated with immunosuppression

118
Q

Horner Syndrome

A

Clinical Presentation: ptosis, anhidrosis, and flushing of affected side of face, miosis (pupillary constriction)
MOA: sympathetic denervation of the face
*associated with spinal cord lesion above T1 and pancoast lung tumor compression of superior cervical ganglia

119
Q

Bitemporal Hemianopsia (Tunnel Vision)

A

Clinical Presentation: loss of temporal vision

MOA: lesion within the optic chiasm (often due to pituitary tumor)

120
Q

Anton’s Syndrome

A

Clinical Presentation: blindness but the patient doesn’t realize they are blind
MOA: damage to the visual cortex and the visual association cortex

121
Q

Pterygium

A

Clinical Presentation: obscured vision; common in elderly
MOA: vascularized conjunctival tissue may grow over the iris obscuring vision
Tx: surgical excision; may recur

122
Q

Corneal Abrasion

A

Extremely common; pt has a scratch of the cornea and feels like there is something in there eye, but has conjunctivitis

123
Q

Uveal Tract Melanoma

A

Arises from melanocytes of nevi in the uvea; hematogenous metastasis usually to liver
Histo: spindle cells that are fusiform in shape; epithelioid spheroid cells with cytoplasmic irregularity
Tx: enucleation or radiation; good prognosis if found early

124
Q

CN III Damage

A

Clinical Presentation:
Motor - ptosis, down and out gaze
Parasympathetic - diminished or absent pupillary light reflex, blown pupil, often with down and out gaze
MOA:
Motor - decreased diffusion of O2 and nutrients to interior fibers from compromised vasculature on the outside of the nerve
Parasympathetic - compression of the nerve (i.e. form aneurysm to PCA or superior cerebellar artery, or uncal herniation); affects fiber s on the periphery first

125
Q

Post Herpetic Neuralgia

A

Clinical Presentation: persistent pain despite resolution of active infection; association with numbness
MOA: presumed secondary to decreased modulation from de-afferentiation of A-beta fibers allowing C fibers to be sensed more
*risk reduced with early use of antivirals

126
Q

Anosmnia

A

Clinical Presentation: loss of sense of smell, can be temporary or permanent
MOA: head trauma can cause shearing of olfactory nerves as they pass through the cribiform plate
*association with early Parkinson’s, Alzheimer’s, MS, and Huntington’s

127
Q

CSF Rhinorrhea

A

Fracture of the cribiform plate can cause leakage of CSF into the nose

128
Q

Sinusitis

A

Clinical Presentation: tapping on bone superficial to sinus will elicit pain
MOA: inflammation of one or more of the paranasal sinuses usually due to bacterial infection secondary to virus or allergies

129
Q

PTSD

A

Clinical Presentation: avoidance of triggers, emotional numbness, persistent arousal; duration of longer than 1 month
MOA: exposure to a traumatic event that is relived and re-activates the anxiety/stress response
Tx: CBT (cognitive behavioral therapy), SSRI, vanlafaxine (SNRI)

130
Q

Acute Stress Disorder

A

Clinical Presentation: avoidance of triggers, emotional numbness, persistent arousal; duration of less than 1 month
MOA: exposure to a traumatic event that is relived and re-activates the anxiety/stress response
Tx: CBT (cognitive behavioral therapy)

131
Q

OCD

A

Clinical Presentation: compulsive behaviors, obsessions that are irrational/excessive; produces dysfunction
MOA: Obsessions - recurrent thoughts, impulses, and/or images
Compulsions - repetitive behaviors that one feels drive to perform
Tx: CBT, SSRI, clomipramine

132
Q

Panic Disorder

A

Clinical Presentation: concern, worry, or change in behavior due to fear of additional attacks for 1 month or longer
MOA: recurrent non-triggered panic attacks with rapid experience of anxiety and physical manifestations
*Has at least 4 of the following: palpitations, paresthesia, depersonalization, abdominal distress, nausea, intense fear, chest pain, choking, chills, sweating, SOA

133
Q

Generalized Anxiety Disorder

A

Clinical Presentation: restlessness, easily fatigues, difficulty concentrating, irritability, sleep disturbances
MOA: excessive worry about multiple events or activities; subjective difficulty redirecting worry
Tx: CBT, SSRI, SNRI, Buspirone, TCA, Benzodiazepines

134
Q

Social Anxiety Disorder

A

Clinical Presentation: exposure provokes immediate anxiety and those situations are endured with distress; is excessive or unreasonable
MOA: fear of one or more social/performance situations; perception of scrutiny by others

135
Q

Insomnia

A

Often a learned behavior component; trouble with the initiation and maintenance of sleep

  • Anxiety can be associated with initiation of sleep
  • Depression can be associated with the maintenance of sleep
136
Q

Parasomnia

A

Clinical Presentation:

  1. Sleep inertia - difficult transition from sleep to wakefullness
  2. Slow wave sleep behaviors - sleep: walking, talking, eating, terrors, periodic leg movements while asleep
  3. REM sleep disorder - failure of REM paralysis mechanism
137
Q

Narcolepsy

A

Clinical Presentation: daytime sleepiness, cataplexy, sleep paralysis, hypnagogic hallucinations may accompany sleep paralysis
MOA: abnormality in brain systems that produce atonia during REM; may involve immune system attack; immediately enter REM when first going to sleep
*cataplexy = abrupt and reversible loss of muscle tone elicited by strong emotion

138
Q

Ramsay Hunt Syndrome (Herpes Zoster Oticus)

A

Clinical Presentation: painful vesicles within the auditory canal, ear drum, and anterior 2/3 of tongue; paralysis of facial muscles and alters taste
MOA: herpes zoster virus reactivation and infection of geniculate ganglia of the facial nerve
Tx: antiviral medications, steroid, pain medications

139
Q

Epilepsy

A

Clinical Presentation: An intrinsic tendency of the brain to have seizures. Defined by two or more unprovoked seizures
MOA: Focal (localization related) - localized EEG abnormalities, structural lesion (often cryptogenic)
Generalized (non-localization related) - often genetic
*anti-epileptic drugs, epilepsy surgery, electrical stimulation of nervous system

140
Q

“Reflex Sympathetic” Dystrophy

A

Clinical Presentation: excessive hyperpathia/allodynia after an injury
MOA: associated with vasomotor changes after an injury. Usually after a period of immobilization. Extreme abnormal sensitization.
*also called Complex Regional Pain Disorder and Causalgia (if associated with a nerve injury)
Tx: aggressive mobilization and pain control

141
Q

Cerebral Palsy

A 
Clinical Presentation: Disorder of movement or posture. Brain lesions do not progress, but clinical manifestations can
MOA: Encephalopathy (brain lesion), acquired early
Sub-classifications:
- Spastic CP (UMN)
- Ataxic CP (Cerebellar systems)
- Dyskinetic CP (Basal Ganglia)
- Hypotonic CP (LMN)
*Diagnosed before age 3
142
Q

Autism

A

Clinical Presentation: Impaired socialization. More than half associated with intellectual disability. Lack of mutual attention, lack of understanding the mental state of others
MOA: Not known, but strong genetic component. More common in males so possibly X linked
Brain changes in: orbitofrontal cortex, anterior cingulate cortex, amygdyla
*Diagnosed before age 3

143
Q

Intellectual Disability

A

Clinical Presentation: Intelligence substantially below average (< 70)
MOA: 33% from unknown causes. Known causes include down’s syndrome, fragile X syndrome, Rett Syndrome, malnutrition, toxin exposure (lead), neonatal injury
*Diagnosed before age 18

144
Q

Autism Spectrum Disorder

A

Impaired socialization that can either be mild with no intellectual disability (Asperger Syndrome) or with severe intellectual disability
*Diagnosed after age 3

145
Q

Convulsion

A

Involuntary, coarse, usually semi-rhythmic, synchronous movements of the limbs. Can be tonic or clonic. Often associated with loss of consciousness.

146
Q

Seizure

A 
Clinical manifestations of abnormal synchronous discharge of (cerebral cortical) neurons. Can be focal onset (old term: partial) or general onset (old term: primary generalized). 
Focal Categories:
1. Aware (simple partial)
2. Impaired Awareness (complex partial)
      a. both 1 and 2 can be 
          motor or non-motor
3. Focal to Bilateral Tonic-Clonic (secondary generalized)
Generalized Categories:
1. Motor
      a. tonic-clonic ("grand mal")
      b. other motor
2. Non-motor (absence, "petit mal")
*Often manifested by convulsions

Brain & Behavior Extras (5 decks)

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