Neurology Cram B And B

Front 1

Nucleus in the hypothalamus charge of saciety center

Back 1

Ventromedial Nucleus

Front 2

Nucleus in the hypothalamus in charge of Hunger and angry center

Back 2

Lateral Nucleus

Front 3

Nucleus in the hypothalamus in charge of cooling and parasympathetic

Back 3

Anterior Nucleus

Front 4

Nucleus in the hypothalamus in charge of Heating and sympathetic

Back 4

Posterior Nucleus

Front 5

Nucleus in the hypothalamus in charge of Circadian rhythm and works in conjunction with the pineal gland

Back 5

Suprachiasmatic Nucleus

Front 6

Nucleus in the hypothalamus in charge of synthesize ADH

Back 6

Supraoptic Nucleus

Front 7

Nucleus in the hypothalamus in charge of synthesize Oxytocin

Back 7

Paraventricular Nucleus

Front 8

Nucleus in the hypothalamus in charge of sexual behavior and release GnRH

Back 8

Preoptic Nucleus

Front 9

An injury in the lateral Nucleus of the hypothalamus will make you do what?

Back 9

Stop eating, will never get hungry.

Front 10

An injury in the ventromedial Nucleus of the hypothalamus will make you do what?

Back 10

Eternal Hunger, hyperphagia, weight gain

Front 11

Explain the mechanisms of fever and the thermoregulation.

Back 11

Fever is triggered by pyrogens and inflammatory proteins Il-1, Il-6, and TNF. Stimulated by prostaglandin E2. This increases the anterior hypothalamus set point causing hyperpyrexia.

Front 12

All sensory information goes through the thalamus except?

Back 12

Smell

Front 13

What are the 6 most important thalamic nuclei

Back 13

Ventral posterolateral (VPL)

Ventral posteromedial (VPM)

Lateral geniculate Nucleus (LGN)

Medial geniculate Nucleus (MGN)

Ventral Lateral (VL)

Pulvinar nucleus

Front 14

What dos the VPL in the thalamus do? What's the input, and the output locations?

Back 14

Process all sensory information (Pain, temperature, touch, proprioception, vibration)

Imput: spinothalamic tracts, Dorsal column medial lemniscus pathway.

Output: somatosensory cortex

Front 15

What dos the VPM in the thalamus do? What's the input, and the output locations?

Back 15

All sensory information to the face and taste

Input: trigeminal and gustatory

Output: somatosensory cortex

Front 16

What dos the LGN in the thalamus do? What's the input, and the output locations?

Back 16

It process vision information

Input: CNII

Outout: Calcarine sulcus

Front 17

What dos the MGN in the thalamus do?

Back 17

Process hearing information

Front 18

What dos the VL in the thalamus do? What's the input, and the output locations?

Back 18

Motor information

Input: basal ganglia

Output: Motor Cortex

Front 19

What happens in a thalamic syndrome?

Back 19

Usually by a Lacunar stroke

Contralateral sensory loss of Face, arms, legs on all sensory modalities.

Can lead to long term chronic pain

Front 20

Loss of ADH from the hypothalamus can lead to what type of diabetes?

Back 20

Diabetes insipidus

Front 21

What relation does a craniopharingioma have with the hypothalamus?

Back 21

Rare tumor in children

Put pressure on the optic chiasm and can cause Bitemporal hemianopia

Put pressure on the hypothalamus

Can cause hypothalamic syndrome

Front 22

What can you see on a hypothalamic syndrome?

Back 22

Diabetes insipidus (Loss of ADH)

Fatigue (loss of CRH- low cortisol)

Obesity

Loss of temperature regulation

Front 23

What does the vestibular system does? And where its located?

Back 23

Its located in the central portion of the inner ear.

Contains system for balance, posture, and equilibrium.

Coordinates head and eyes movement

Front 24

What are 3 typical symptoms of vestibular dysfunction?

Back 24

Vertigo

Nystagmus

Nausea/Vomiting

Front 25

Describe peripheral vertigo and what can cause it?

Back 25

Normal nystagmus

Positional testing: Delayed nystagmus

Normal proprioception

Stable romberg

Peripheral = usually Benign

Inner ear problem

Normal nystagmus

Benign positional vertigo

Vestibular neuritis

Meniere's disease

Front 26

Whats the triad of Meniere's?

Back 26

Tinnitus

Hearing loss

Vertigo

Front 27

Describe central vertigo and what can cause it?

Back 27

Usually fatal, bad or poor prognosis

Upbeat or downbeat nystagmus

Positional testing: IMMEDIATE Nystagmus

Skew deviation: vertical misalignment of the eyes

Diplopia

Dysmetria (ataxia)

Other CNS symptoms

Brainstem or cerebellar lesion

Brainstem Stroke

Cerebellar infarction or hemorrhage

Tumor posterior fosa

Front 28

Whats vestibular neuritis?

Back 28

Neuropathy of the vestibular portion of the CN VIII

Benign, self limited

Usually viral, or post inflammatory

One of the Cause of vertigo

Front 29

What does the cerebellum do?

Back 29

Aids in coordination and balance

Front 30

What's the input to the cerebellum?

Back 30

Contralateral cortex via the middle cerebellar peduncle

Ipsilateral propioceptive via the inferior cerebellar peduncle

Front 31

What's the output of the cerebellum? And what type of cells go through it?

Back 31

Via the upper cerebellar peduncle via the Purkinje cells and the deep cerebellar nucleis

Front 32

What are the names and the pnemotecnic of the deep cerebellar nucleus?

Back 32

DON'T EAT GRASY FOOD

D= DENTATE

E= EMBOLIFORM

G= GLOBOSE

F= FASTIGIAL

Front 33

Which of the deep cerebellar nucleus is the only one lateral?

Back 33

Dentate

Front 34

Lateral lessions of the cerebellum affect voluntary movements of what parts of the body?

Back 34

Lateral structures (Extremities)

Front 35

Medial lesions of the cerebellum will give you problems of what type?

Back 35

Truncal ataxia, nystagmus, head tilting

Front 36

Name of the protein that its damage in Friedrichs Ataxia?

Back 36

Frataxin

Front 37

What cause Friedrichs Ataxia at a genetic standpoint?

Back 37

A mutation in the FXN gene, where there's an abnormal repetition of a GAA sequence within the gene.

The triplet repeat normally 34 times, pathologically is repeated +100>

Front 38

Autosomal recessive disorder that affects neurons , cardiomyocytes, and pancreatic Beta Cells.

Back 38

Friedrichs Ataxia

Front 39

What happens in Friedrichs Ataxia at a biochemistry level?

Back 39

•Low levels of frataxin

•No conversion of iron to iron-sulfur cluster

•Low levesl of ATP means low energy

•Increase in iron levels inside the cell wich react with oxygen and creates oxygen radicals (Oxidative Damage)

•DEATH OF THE CELL

Front 40

Ataxia, Hypertrophic Cardiomyopathy, Diabetes mellitus are common in which pathology?

Back 40

Friedrichs Ataxia

Front 41

What substance is deficient in the Wernicke-Korsakoff syndrome?

Back 41

Vitamin B1 or thiamine

Front 42

What's the acute reversible stage of the Wernicke-Korsakoff syndrome?

Back 42

Wernicke's Encephalopaty

Front 43

How many types of hydrocephalus are? And name them

Which thing mimic a Hydrocephalus?

Back 43

3

•Comunicating hydrocephalus

• Non communicating hydrocephalus

• Normal pressure Hydrocephalus

•Ex Vacuo hydrocephalus (Mimics)

Front 44

What happens in communicating hydrocephalus? And clinical presentation?

Back 44

Low CSF absorption by the arachnoid granulations

•Increase ICP

•Papilledema

•Herniation

Front 45

What happens in non communicating hydrocephalus?

Back 45

Caused by structural blockages of CSF circulation within the ventricular system

Front 46

What happens in normal pressure hydrocephalus? And clinical presentation?

Back 46

Affects the elderly, idiopathic, CSF pressure elevated only episodically

Expansion of the ventricles distorts the fibers of the Corona Radiata and give rise to the typical symptoms.

•Urinary incontinence

•Gait apraxia

•Cognitive disfunction

Front 47

A patient that its wet, wobbly, and wacky has what disease?

Back 47

Normal pressure hydrocephalus

Front 48

What happens in Ex Vacuo ventriculomegaly? And what diseases show this type of condition?

Back 48

Appearance of increase volume in CSF on imaging, but its actually due to decreased brain tissue and neuronal atrophy , but ICP is normal and the triad of NPH is not seen.

•ALZHEIMER

•Advance HIV

•Picks disease

•Huntington

Front 49

What happens in Multiple sclerosis?

Back 49

Autoimmune inflammation and desalination of CNS.

Front 50

Acute optic neuritis painful and unilateral, Marcus Gunn pupil, fatigue, scanning speech, intention tremor, nystagmus and INO. Symptoms may exacerbate with increased body temperature and more common in women in their 20s and 30s?

Back 50

Multiple sclerosis

Front 51

Common lab findings in multiple sclerosis?

Back 51

+IgH levels and basic protein levels in CSF spinal tap.

MRI is gold standard and see periventricular plaques

Front 52

What happens in pseudotumor cerebri?

Back 52

•Idiopathic intracranial hypertension

•+ICP without tumor or other cause

•Intractable disabling headache

•Papilledema and visual loss

•Pulsatil tinnitus (Rushing water or wind)

Front 53

What happens in berry or secular aneurysms? And its associated to what conditions? And most common sites?

Back 53

Rupture of the aneurysm and intracranial bleed. Most common in Anterior communicating arterie and posterior communicating arteries. Associated to ADPKD and Ehlers-Danlos syndrome

Front 54

If a berry aneurysm grows large enough near the Acom what can compression do?

Back 54

Bitemporal hemianopia due to compression of the optic chiasm

Front 55

If a berry aneurysm grows large enough near the PCom what can compression do?

Back 55

Ipsilaterap CNIII plays with blown pupil

Front 56

What's a charcot-Bouchard microaneurysm? And what zones affect?

Back 56

An aneurysm associated with chronic hypertension and affects small vessels (Lenticulostriate arteries) in basal ganglia and thalamus

Front 57

Which are the 5 nuclei of the basal ganglia?

Back 57

•Substantia Nigra

•Subthalamic Nucleus

•Putamen

•Caudate Nucleus

•Globus Pallidus

Front 58

Huntington's affects which part of the basal ganglia?

Back 58

Striatum

Front 59

In Wilson's disease which part of the basal ganglia is affected?

Back 59

GP internus

Striatum

Front 60

In Parkinson's disease which part of the basal ganglia is affected?

Back 60

Substantia Nigra

Front 61

In Hemiballism which part of the basal ganglia is affected?

Back 61

Subthalamic Nucleus

Front 62

Whats the protein that induces the ectoderm to differentiate into neuroectodern and form the neural plate?

Back 62

Sonic hedgehog

Front 63

The neuroepithelia give rise to which type of cells?

Back 63

CNS neurons

Ependymal cells

Oligodendrocytes

Astrocytes

Hint 63

4

Front 64

The neural Crest give rise to which cells?

Back 64

PNS neurons

SCHAWANN cells

Glia

Melanocytes

Adrenal medulla

Hint 64

5

Front 65

What are the different types of spina bifida? Which is the most common? Which is the most severe?

Back 65

•Spinna bifida occulta (Most common)

•Meningocele

•Mielomeningocele (Most severe)

Front 66

Describe spina bifida occulta

Back 66

Failure of caudal neuropore to close, but no herniation. Dura is intact . Tuff of hair or skin dimple at the level of the bony defect

Front 67

Describe the meningocele?

Back 67

A type of spina bifida in which only the meninges herniate through the bony defect but not neural tissue.

Front 68

Describe myelomeningocele

Back 68

A type of spina bifida in which meninges and neural tissue herniate through the bony defect.

Front 69

What's a Myeloschisis?

Back 69

Also called rachischisis, Exposed unfused neural tissue without skin covering

Front 70

Describe Anancephaly and what's a common clinical findings during pregnancy?

Back 70

Failure of the rostral neuropore to close leads to no forebrain. The clinical finding associated with it is polyhydramnios because there's no swallowing center in the brain.

Front 71

What's holoproscencephaly? In what time this occurs? Suspected because a mutation where?

Back 71

Failure of the embryonic forebrain to separate into 2 cerebral hemispheres.

Usually weeks 5-6

Related to a mutation in the sonic hedgehog signaling pathway.

Front 72

What are common defects of holoprosencephaly?

Back 72

Associated to midline defects like

Cleft lip/palate (Moderate form)

Cyclopia (severe form)

Front 73

Open neural tube defects are associated with an increase in what proteins?

Back 73

+AFP

+AChE

Front 74

Describe chiari malformation type 1.

Back 74

Ectopia of cerebellar tonsils, congenital, usually asymptomatic in childhood and manifest during adulthood as headache and cerebellar symptoms.

Associated to syringomyelia

Front 75

Describe chiari malformation type 2

Back 75

Herniation of the cerebellar tonsils and vermis, acqueductal stenosis leads to a non communicating hydrocephalus. Associated with myelomeningocele . More severe than type 1, and present in early life.

Front 76

What's a Dandy Walker malformation ?

Back 76

Agenesis of the cerebellar vermis, cyst enlargement of the 4th ventricle. Associated with non communicating hydrocephalus.

Front 77

Describe syringomyelia!!!

Back 77

Cyst cavity within central canal of the spinal cord, fibers crossing the anterior white commisure are typically damaged first. Associated with chiari malformation type 1 and watch for a possible Horner's syndrome in questions due to lateral horns affected.

Front 78

Whats the common clinical finding of syringomyelia?

Back 78

Cape like bilateral, symmetrical loss of pain and temperature sensation in upper extremities.

Front 79

Whats chromatolysis? And what are de physical characteristic seen in the cell?

Back 79

Reaction of neuronal cell body to axonal injury. Theres an increase in protein synthesis in effort to repair the damage axon.

Round cellular swelling

Displacement of the nucleus to the periphery

Dispersion of the Nissl substance through cytoplasm.

Front 80

Describe CN1

Back 80

Smell, only CN without thalamic relay to cortex

Front 81

Describe CN2

Back 81

Optic nerve (sight)

Front 82

Describe CN3 and what happens in a CN3 palsy?

Back 82

Oculomptor nerve

Eye movement (SR, MR, IR, IO)

Pupillary constrictor

Eyelid opening

Eye down and out, pupil dilated, and ptosis

Front 83

Describe CN4 and CN4 palsy?

Back 83

Trochlear Nerve

Eye movement (SO)

Can't look stairs or read

Eye up and inward in a CN4 palsy

Pupil is higher in affected side

higher in affected side

Front 84

Describe CN5 and a palsy

Back 84

Trigeminal nerve

Masticating muscles

Sensory to the face via 3 branches

(Mandibular, maxilar, ophthalmic)

Somatosensory from 2/3 anterior part of tongue

Dampening of loud noises tensor tympani

Palsy: numb face, weak jaw deviated to the affected side, trigeminal neuralgia

Tx: carbamazepine

Hint 84

4 things

Front 85

Describe CN6 and a palsy

Back 85

Abducens nerve

Eye movement (LR)

Palsy: eye inward in primary position

Front 86

Describe CN7 and a Palsy

Back 86

Facial nerve

Motor to the face, taste from 2/3 anterior tonge, lacrimation, salivation, eye closing, auditory modulation via stapedius

Palsy: loss of corneal reflex, loss of taste, hyperacusia, bell's palsy

Front 87

Describe CN8 and palsy

Back 87

Vestibulocochlear nerve

Hearing and balance

Palsy: dolls eyes, hearing and balance problems

Front 88

Describe CN9 and palsy

Back 88

Glossopharyngeal nerve

Taste and sensation of the posterior 1/3 tongue, swallowing, salivation, monitor carotid body and chemo and baro receptors, elevation of pharynx and larynx

Palsy: loss of gag reflex, loss of posterior tonge sensation, trick body into thinking has low BP, ♤Hr, vasoconstriction, and ♡BP

Front 89

Describe CN10

Back 89

Vagus nerve

Swallowing, soft palate elevation, midline uvula, talking, cough reflex, parasympathetic to thoracoabdominal viscera and monitoring aortic arch chemo and baroreceptors

Front 90

Describe CN11 and palsy

Back 90

Accessory nerve

Head turning and shoulder shrugging

(SCM, and Trapezius)

Palsy: Difficulty turning head toward normal side, shoulder drop affected side

Front 91

Describe CN12 and palsy

Back 91

Hypoglossal nerve

Tongue movement

Palsy: tongue deviated to the affected side

Front 92

Cranial nerve reflexes

Back 92

Corneal *CN5 v1

Lacrimation *CN5 v1

Jaw jerk *CN5 v3

Pupillary *CN3

GAG *CN9

Cough *CN10

Front 93

Describe corticospinal tract

Back 93

Front 94

Describe the ascending tracts

Back 94

Front 95

What are the 3 types of ischemic strokes?

Back 95

Thrombotic

Embolic

Hypoxic

Front 96

The hypoxic stroke is commonly during ?

Back 96

Cardiovascular surgeries and affect watershed areas

Front 97

Thrombotic strokes are common where? And why?

Back 97

In the MCA over a ruptured atherosclerotic plaque

Front 98

Treatment and image diagnosis of ischemic stroke?

Back 98

TPA if within 3 to 4.5 hours of onset and sure it's not hemorrhage via MRI or non contrast CT.

Thrombectomy and medical therapy like aspirin and clopidrogrel

Front 99

What's a Transient ischemic attack?

Back 99

Brief, reversible episode of focal neurologic disfunction without acute infarction. (-) in the MRI almost all resolve in less than 15 minutes by themselves.

Front 100

Aging related impaired accommodation focusing on near objects needing reading glasses

Back 100

Presbyopia

Front 101

What happens in hyperopia and how it is the eye?

Back 101

Eye is too short and light is focused BEHIND the retina

Front 102

What happens in myopia and how it's the eye?

Back 102

Eye is too long and light is focused IN FRONT of the retina

Front 103

What's astigmatism? And where it is located the refractive power in this pathology?

Back 103

Abnormal curvature of the cornea and has multiple focal points in the retina

Front 104

Describe age related macular degeneration!

Back 104

2 types

Dry 80%: Deposition of yellowish material (Drusen) in between Bruch membrane and retinal pigmented epithelium.

Slow and gradual loss of vision

Wet 10% -15%: rapid loss of vision due to bleeding 2dary to choroidal neovascularization.

Front 105

Back 105

Age related macular degeneration

Front 106

Back 106

Diabetic retinopathy

Front 107

Describe diabetic retinopathy

Back 107

Two types

Non proliferative: 95% damage capillaries leaks blood into the retina, lipids in the retina, hemorrhage and macular edema

Proliferative: 5% Chronic hypoxia resulting in new blood vessels and retinal detachment

Front 108

Back 108

Hypertensive retinopathy

Front 109

Describe hypertensive retinopathy

Back 109

Retinal damage due to chronic uncontrolled Hypertension.

Front 110

Back 110

Retinal vein occlusion

Front 111

Describe retinal vein occlusion

Back 111

Blockage of veins due to compression of nearby arterial atherosclerosis. Retinal hemorrhage and venous engorgement.

Front 112

Back 112

Retinal detachment

Front 113

Describe retinal detachment

Back 113

Separation of neurosensory layer of the retina (Rods and cones) from the outermost pigmented epithelium. Degeneration of photoreceptors leads to vision loss like a curtain drawn down . It's a surgical emergency.

Front 114

Back 114

Central retinal artery occlusion

Front 115

Describe central retinal artery occlusion

Back 115

Acute painless monocular vision loss with cherry red spot on the fovea. Think of embolic source.

Front 116

Back 116

Retinitis pigmentosa

Front 117

Describe retinis pigmentosa

Back 117

Inherited progressive retinal degeneration. Night blindness with bone and spicule shaped deposits

Loss of photoreceptors. Legally blind by the age of 40

Rods affected first

Front 118

Describe papilledena

Back 118

Optic disc swelling usually bilateral due to ♤ICP. Enlarge blindspot and elevated optic disc swelling with blurred margins

Front 119

Back 119

Papilledema

Front 120

Describe conjunctivitis and the types

Back 120

Inflammation of the conjunctiva-- red eye

3 types:

•Allergic: itchy eyes, bilateral

•Bacterial: pus, treat antibiotic

•Viral: most common, often adenovirus, sparse mucous discharge, ♤lacrimation, self resolving

Front 121

Describe cataracts

Back 121

Painless opacification of the lens, often bilateral, resulting in glare and ♡vision loss especially at night.

Front 122

Risk factors for cataracts?

Back 122

Old age

Alcohol abuse

Diabetes mellitus

Smoking

Excessive sunlight

Prolonged corticosteroids use

Trauma

Infections

Hint 122

8

Front 123

Congenital risk factors of cataracts?

Back 123

Galactosemia

Galactokinase deficiency

Trisomy 13,18,21

Torch infections

Marfan syndrome

Alport syndrome

NF type 2

Front 124

Back 124

Cataracts

Front 125

Describe the Polyol Pathway of cataracts

Back 125

♤ in glucose leads to increase in sorbitol. Sorbitol converts to fructose but it's a slow process that leads to acumulation of sorbitol and eventually opacification of the lens.

Front 126

Back 126

Uveitis with hypopyon

Front 127

Describe uveitis

Back 127

Inflammation of the uvea, name based on the location of the inflammation.

Anterior uveitis : iritis

Posterior uveitis: choroiditis or retinitis

Front 128

What's hypopyon? And its associated with what?

Back 128

Accumulation of pus in anterior chamber of the eye. Associated with systemic inflammatory disorders like sarcoidosis, arthritis rheumatoid etc....

Front 129

After how much time of ischemia theres irreversible damage in the brain?

Back 129

5 minutes

Front 130

Most vulnerable areas of the brain in case of ischemia and what's the pnemotecnic?

Back 130

Vulnerable hippos needs pure water

Vulnerable Hippocanpus

Neocortex

Purkinje cells

Watershed areas

Front 131

Whats the Pathophysiology of Myasthenia gravis?

Back 131

85% of cases involves autoantibodies directed against postsynaptic acetylcholine receptors (AchR), thereby impairing neuromuscular transmission.

10–15% of cases are associated with thymoma.

Front 132

Autoimmune neuromuscular disease characterized by generalized muscle weakness. Women are more frequently affected and about 10–15% of cases are associated with thymoma. The most common initial symptoms are ptosis and/or diplopia due to ocular muscle weakness, with the disease usually progressing to generalized weakness within two years.

Back 132

Myasthenia Gravis

Front 133

Clinical presentation of Myasthenia gravis?

Back 133

Muscle weakness worsens throughout the day with increased activity and improves after rest.

Front 134

Treatment of choice for Myasthenia gravis?

Back 134

Acetylcholinesterase inhibitors, possibly in combination with immunosuppressive drugs

Front 135

Chronic, degenerative disease of the CNS that is caused by an immune-mediated inflammatory process. This process results in the demyelination of white matter in the brain and spinal cord.

Back 135

Multiple Sclerosis

Front 136

What type of immune mediated inflammatory process is Multiple sclerosis?

Back 136

Type 4

Front 137

What type of immune mediated inflammatory process is Myasthenia Gravis?

Back 137

Type 2

Front 138

Investigation of choice for the diagnostic of MS?

Back 138

Brain and spine MRI with Multiple sclerotic plaques in periventricular areas

Front 139

What's a Migrane?

Back 139

headache characterized by recurrent episodes of unilateral, localized pain that are frequently accompanied by nausea, vomiting, and sensitivity to light and sound.

Front 140

Injury of the upper trunk of the brachial plexus (C5-C6) cause what type of palsy?

Back 140

Erb palsy

Front 141

Weakness of muscles in the C5 and C6 myotomes → flexed wrist with an extended forearm and internally rotated and adducted arm (waiter's tip posture)

Back 141

Erb palsy

Front 142

Injury to the lower trunk of the brachial plexus (C8–T1) cause a what palsy?

Back 142

Klumpke palsy

Front 143

Weakness of muscles in the C8 and T1 myotomes (intrinsic hand muscles) → total claw hand

Back 143

Klumpke palsy

Front 144

Pelvic Ring fracture with sensory deficits on Medial thigh its an injury on what nerve?

Back 144

Obturator nerve injury

Front 145

A lumbar disc herniation between the vertebral bodies L5 and S1 is a common cause of S1 radiculopathy, which can manifest with?

Back 145

Weak achilles tendon reflex

Front 146

Diminished sensation of the anterior lateral thigh is consistent with an injury to wich Lumbar region?

Back 146

L3 Radiculopathy

Front 147

Difficulty walking on heels (e.g., foot drop) may be seen in patients with an injury to wich root nerves?

Back 147

L4 or L5 nerve roots

Front 148

Which vitamin deficiency is commonly seen in association with isoniazid (INH) use in antituberculosis treatment?

Back 148

Pyridoxine (vitamin B6)

Front 149

In a immunocompromised patient, multiple ring enhancing lesions within the subcortical white matter, basal ganglia, and/or thalamus are highly suggestive of

Back 149

Cerebral toxoplasmosis

Front 150

Patients with inherited retinoblastoma gene (Rb gene) mutations and Leucokoria have a significantly increased risk of developing

Back 150

Osteosarcomas

Front 151

The earliest sites of neurodegeneration in Alzheimer disease are structures in the medial temporal lobe such as the ___________, __________,which are critical for memory formation.

Back 151

hippocampus and parahippocampal cortex

Front 152

Orthostatic hypotension, livedo reticularis, peripheral edema, and ataxia are sings toxicity of what medication in a newly diagnosed parkinson patient?

Back 152

Amantadine Toxicity

Front 153

Mechanism of action of Amantadine?

Back 153

Amantadine increases dopamine release, decreases dopamine reuptake, and inhibits the N-methyl-D-aspartate (NMDA) receptor.

Front 154

ATP-dependent motor protein responsible for the retrograde migration and movement of cellular organelles and proteins along microtubules in axons used by rabies virus to infect the CNS

Back 154

Dynein

Front 155

Wich is the mechanism of action of triptans, which are considered first-line abortive therapy for the treatment of acute migraine headaches and cluster headache attacks?

Back 155

Activation of 5-HT1 receptors

Front 156

Is a common complication of axillary lymph node dissection, it present with winged scapula caused by paralysis of the serratus anterior muscle.

Back 156

Long thoracic nerve injury

Front 157

is the most common parasitic disease of the nervous system and the most important cause of adult-onset seizures in Asia, Africa, Central and South America

Back 157

Neurocysticercosis by Taenia solium

Front 158

Most common cause of anti-Yo antibody-associated PCD in women

Back 158

Breast cancer

Front 159

In Huntington Disease the mutation is on which chromosome?

What neurotransmiser is increased and which is decreased?

Back 159

Chromosome 4

Increased Dopamine Levels

Decreased Ach, and Gaba