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USMLE Step 2 - Top 5% > Neurology šŸ§  > Flashcards

Neurology šŸ§  Flashcards

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USMLEĀ® Step 1 flashcards
1
Q

What is a more specific and sensitive test for CZJ

A

RT QulC test. Real time quaking induced conversion test

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2
Q

Dx this:
2mo Hx of -
More sleep, withdrawn, cognifitive issues, balance issues, dysmetria, homonymous hemianopia, wide gait. CT ok

A

CZJ

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3
Q

What is Lennox Gastaut

A

A seizure disorder. Presents usually below 5. Seizures and learning difficulties. Slow Spike and wave pattern on EEG.

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4
Q

What is miller fisher, and how to Tx

A

Miller Fisher syndrome (MFS) is a rare neurological disorder that is considered a variant of Guillain-BarrƩ syndrome (GBS). It is characterized by a triad of symptoms, including Ataxia (lack of coordination), Areflexia (absent reflexes), and Ophthalmoplegia (weakness or paralysis of the eye muscles). Tx same as GBS

British Breslin of Guillain Barre ā€œAOOā€

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5
Q

Boy falls on toothbrush and then gets hemiplegia and hemianeatstesia. Dx? How to confirm Dx?

A

Carotid arteryā€™s dissection. Dx with CTA or MRA

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6
Q

Main criteria for thrombectomy

A

More than 4.5 hours since stroke (means tPA cannot be used). There is large vessel occlusion found on CTA. Neurological dysfunction.

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7
Q

Patient has stroke, less thAn 4.5 hoursā€¦ what to do

A

tPA

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8
Q

Patient has stroke, more than 4.5 hoursā€¦. Less than 24. Do what next

A

Do CTA to check for LVO. If present do thrombectomy

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9
Q

Concussion Managment

A

Neuro exam, rest 24hrs, lower screen time, grandual return to activity (start with light aerobic stuff). No CT unless alarming signs

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10
Q

These are signs of?
Impact on externally rotated , abducted arm. Now sits in that position. Pain. Shoulder asymmetry. Ancillary fullness.

A

Anterior shoulder dislocation

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11
Q

List the biggest risk factor for stroke

A

HTN. Then smoking, then DM, the hyperchol

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12
Q

Mx for familial macrocephaly

A

Reassure and observe. This is where patient has head circ above 97th percentile. No syndrome, infx, hydrocephalus etc.

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13
Q

Vertigo, unilateral dysmetria, that is sudden onset and persistent. What is the likely cause

A

Stroke

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14
Q

Mx for FT dementia

A

Behavioural intervention. Consider SSRIs for overt behaviour

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15
Q

Vascular dementia has prominent deficits in what?

A

Cognition

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16
Q

What will be seen on a CT and MRI for diffuse axonal injury

A

CT is often negative. MRI will show grey ā€“ white matter differentiation loss and punctate haemorrhageļæ¼

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17
Q

How can a patient get median nerve palsy from brachial artery cannulation

A

It can occur due to laceration from the sharp, or compression from a local haematoma. The compression will most likely just be sensory deficit, and reversible. Whereas the laceration will be both motor and sensory deficit

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18
Q

When do we consider prophylactic medication for tension headaches

A

Is the patient is having more than one headache a month, we consider giving TCA. Obviously stress reduction techniques are important to

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19
Q

Dx this:
Fever, lower motor neurone signs, focal tender back pain, a little slipped disc-like signs.

A

Epidural abscess

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20
Q

How to Dx and Tx epidural abscess

A

MRI, and broad spec Abx/aspirate

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21
Q

What stroke signs suggest emboli origin

A

Sudden and maximal at onset. Many vascular territories can be affected. Risk factors like AF or heart issues.

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22
Q

Dx this:
30 year old. Severe headache. Had Hx of milder episodic right sided headaches. ICP signs.

A

Ruptured AVM

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23
Q

What can be given to reduce peritumour edema in brainCA

A

IV GCs

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24
Q

Main Mx of cerebellar haemorrhage.and what are the indications to do this

A

Surgical decompression, do if Neuro issues, obs hydrocephalus, AMS, BS compressed, more than 3cm hem

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25
Q

Dx this: and Tx:
Young woman, numb in both arms and legs. And weak in arms and legs too. No sensation below neck. MRI shows increase T2 signal in C. Spine, and no masses.

A

Transverse myelitis. Give IV CS

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26
Q

NEXUS criteria for doing imaging on neck

A

Neuro issues, intoxicated, tender spine, AMS, obvious injury. Need only 1

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27
Q

If an old person has main difficulty hearing/understanding what someoneā€™s saying, especially in crowded areasā€¦ sign of what

A

Presbycusis. Concinents are high frequency, so this makes it hard to understand people.

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28
Q

diagnostic test for pseudotumour cerebra, and what must be done prior to this

A

Elevated pressure on LP is diagnostic. But do CT or MRI prior to rule out lesion

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29
Q

Big risk in pseudotumour cerebri. What can be done to prevent

A

CNII compression and blindness. Other than normal Tx, can do CNII sheath fenestration

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30
Q

Dx this

Agilent has low concentration, poor sleep, fatigue, headaches, dizziness for a month following post concussion.

A

Post concussion syndrome

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31
Q

How to distinguish thunderclap from SAH and pituitary apoplexy

A

Apoplexy can affect ACTH and cause drop in BP. CNIII often involved. History of adenoma (headache, lossed libido, mense irregularity),. No neck stiffness like SAH

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32
Q

Adult has new seizure. Tonic clonic. What is the initial Invx aim

A

Rule out metabolic and toxicological causes. Then can do imaging (MRI in non emergency, CT in emergency)

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33
Q

cephalohematoma presentation and Mx.

A

At birth. Usually following forcep or vacuum use. Doesnā€™t cross suture lines. Doesnā€™t fluctuate. Is firm. Usually self limited

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34
Q

Caput succedanem presentation and Mx

A

At birth. Boggy and crosses suture lines. Self limited

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35
Q

Subgaleal hemorrhage presentation and Mx

A

At birth. Emissary veins rupture during delivery . Fluctuating scalp mass that crosses suture line.

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36
Q

Tx of homocysteinuria

A

B12, B9, B6 and anticoag

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37
Q

Delerium Tx for elderly patient who is agitated

A

Low dose haloperidol (or atypical if has PD). Bezos CI if elderly

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38
Q

Preventative treatment for migraines in a pregnant lady

A

BB.

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39
Q

What is the PECARN rule

A

Paediatric traumatic brain injury, who gets CT. Anyone with RFs; AMS, LOC, big fall, skull fracture signs, vomiting or severe headache

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40
Q

Neurosyphilis Tx

A

10-14 days of IV penicillin G

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41
Q

Glucocorticoid myopathy (vs other myopathies)

A

After high dose GCs. esr and CK are normal. There is no pain, just weakness. Whereas statin myopathy causes pain. Hypothyroidism causes weakness and pain. Polymyositis causes weekends, rarely pain. Poly myalgia only pain/stiffness, no weakness, and high ESR.

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42
Q

Signs and symptoms of cryptococcal meningitis

A

Subacute meningism. High ICP (clogged CSF flow). Immunosurpressed.

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43
Q

CSF of cryptococcosis

A

Lowish glucose, high protein, lymphocytosis,

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44
Q

Answer this regarding pseudotumour cerebri Tx:

The only disease modifying mx
First line if eye sight not at emergent risk
First line of immediate threat to eye sight

A

Weight Loss

IV CAI

VP shunt or optic nerve fenestrations

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45
Q

Drugs which can precipitate acute closed angle glaucoma

A

AntiCh, Decongestant, antiemetics

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46
Q

Type B thoracic dissection often causes damage to which part of the spinal cord.

A

T10-12. Due to vulnerability to ischemia (adamkeiwicz artery). Dorsal Columns are spared and itā€™s an anterior spinal cord mess!

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47
Q

Describe the whole indication thing for thrombolysis/thrombectomy

A

They are considered independently. So can do both, either or neither. Less than 4.5 hours for tPA, less than 24hrs for thrombectomy. To do thrombectomy, need proof of large vessel involvement, using CTA

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48
Q

What is usually responsible for central cord syndrome.

A

Older patients with an underlying cervical spondylosis, get whiplash (over extension of the neck). Causing central cord issue. Lower limbs ok, bladder bowel ok. Sensory loss and weakness in arms and low reflexes

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49
Q

Can we do anticoag or thrombosis in IE induced stroke? And why? What do we do instead?

A

No, the risk of hemorrhagic transformation is very high, since the infection causes an arteritis. Do IV Abx and removed dodgy valves

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50
Q

Tx for decompression sickness

A

100% O2, trenedlenberg positioning, IV fluid

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51
Q

What is a breath holding spell. What are the types

A

Crying, trauma etc. causes a cessation of breathing. This causes cyanosis (Cyanotic types) or just mild pallor (pallid type). Itā€™s 100% normal. There is a risk it comes from IDA, so check

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52
Q

What is tethered cord

A

Tethered cord is essentially a stretching of the spinal cord. Usually seen in patients with spina bifida, but can also be seen in patient to hyperextend. Usually find progressive gate issues, back pain, continents, lower motor neuron signs, and feet finding such as arched feet and fix flexion of the toes (pes cavus and hammer toe)

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53
Q

What is delayed emergence and emergence delirium after anaesthesia

A

Emergence delirium is a patient who is hyperactive after general A. Delayed emergence is recovering from general A. Longer than the average patient (30-60 mins). Just rest and reassure, rule out serious issues like stroke.

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54
Q

Anatomy of cephalohematoma and subgaleal hemorrhage

A

Cephalohematoma is between the periosteum and skull, making it hard and unable to cross lines. Therefore can just observe and be careful of hyperbili when the blood is resorbed. SubG hem is between the periosteum and galea aponeurosis, so it bleeds quick, crosses lines and is fluctuant.

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55
Q

How can diabetes lead to b12 deficiency

A

Metformin

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56
Q

Cause of diarrhoea following cholecystectomy or bowel resection. If osmotic gap low, and doesnā€™t stop when fasting

A

Secretory (bile acid diahhrea)

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57
Q

Is MS flare more likely in preg or post partum

A

Post partum

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58
Q

What symptoms can precede the focal neuro signs in MS

A

Fatigue

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59
Q

Which eye issue can be seen in sturg weber

A

Glaucoma, due to angle deformity

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60
Q

What is paroxysmal SNS hyperactivity

A

Usually after TBI, the SNS randomly goes into over drive (likely due to damage to centres inhibiting SNS). Often high SNS in times of external stimulation of patient (bathing or repositioning )

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61
Q

Abortive and preventative meds for migraine

A

Abort: NSAID, triptan, antiemetic, ergot

Prevent: topiramate, amitrypt, beta blocker (Esther, Ashley, Amy)

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62
Q

Causes of TG neuralgia

A

MS in the pons, mass near the pons, vascular loop compressing TG nerve (most common)

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63
Q

Tremor with these features

Inconsistent
Abrupt onset
Distractable
Chase the tremour

A

Functional

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64
Q

If a patient has parksinosism and they are on dopamine antagā€¦. Whatā€™s the Dx

A

Drug induced Parkinsonā€™s, so stop the med and the symptoms should go in weeks. Being on a DA antag is a 100% exclusion criteria for ideipathic Parkinsonā€™s.

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65
Q

Febrile seizure Mx

A

Abort if needed. Tx fever. Reassure and discharge

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66
Q

Patient with subacute CD like signs, and has microcytic anemia, depig areas, fragile hair, edema. After gastric bypass

A

Cu def

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67
Q

Red flags and exclusion criteria for Parkinsonā€™s

A

Red flags: early postural instability, early bulbar dysfunction, absent non motor signs, severe orthostasis, symmetry.

Exclusion criteria: PSP, aphasia, anti DA meds, cerebellar signs

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68
Q

Dx this

Low concentration, depression for 6 mo, forgetful and dementia signs. Restless, abrupt facial expression changes, unable to maintain grasp

A

Huntingtonā€™sā€¦. presents as agitation and restlessness early on

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69
Q

Epidural lidocaine toxicity

A

Systemic toxicity, can inhibit the inhibitory neurones. Causing perioral numbness, metallic taste, seizures etc.

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70
Q

Concussion Managment

A

No same day play. Neuro evaluation. Rest for 24 hr. Then start aerobic, to non contact, to contact sports. Low screen time

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71
Q

Nerve supply for the dura. Divide based in anterior/middle, posterior fossi

A

Nerve supply is from CN V (anterior and middle cranial fossa), CN X (posterior fossa), sympathetics, and C1ā€“C3 cervical nerves.

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72
Q

Is the epidural space deeper or superficial to the dura

A

Superficial. Just outside the dura, inside the ligamentum flavum.

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73
Q

Cavernous sinus thrombosis involves which CNs

A

Nerves 4, 5 (2 and 1), 6

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74
Q

CN IV lesion. Head tilts which way

A

Contra lateral

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75
Q

Nerve responsible for muscles of mastication

A

CN V

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76
Q

Diplopia worked when walking stairs and readingā€¦. CN

A

IV.

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77
Q

CNV lesionā€¦ jaw deviates to which side

A

Toward

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78
Q

CNX palsy, uvula deviates which way

A

Away

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79
Q

CNXII palsy, tongue deviates which way

A

Toward

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80
Q

In terms of facial nerve boundaries (upper face and lower face), which does the eye fall into? Relevance to LMN and UMN thing

A

Eye and eyelid is upper face, so eye unable to close if itā€™s a LMN lesion only

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81
Q

Central cord syndromeā€¦ symptoms and explain them.

A

Weakness in the upper limbs due to corticospinal loss medially (arms are represented more medially). Also temp and pain loss bilateral, due to caught decussating fibres of the spinothalamic tract (similar to syrinx damage to the anterior commissure).

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82
Q

Main cause of central cord syndrome

A

Hyperextension of back in elderly, and SC tumours

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83
Q

Other than vascular compression of TG, whatā€™s another common cause of TG neuralgia

A

MS

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84
Q

If trigeminal neuralgia is bilateral, consider what cause

A

MS

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85
Q

Left PCA stroke causes alexia or agraphia

A

Alexia, no agraphia. Cant read, can write

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86
Q

Weber syndrome

A

Potential from PCA stroke. Causing contra lateral hemiparesis, ipsilatera
CNIII palsy and parkinsonian rigidity

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87
Q

Clumpsy hand syndrome is caused by lesions in which area

A

Lacunar infarcts

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88
Q

Patient with oropharyngeal injury, gets horners and neck pain/headache

A

Carotid artery dissection

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89
Q

Most sensitive invx to Dx acute infarct

A

Diffusion weighted MRI

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90
Q

Common causes of venous sinus thrombosis

A

uncontrolled infections of central facial skin, the orbit, or nasal sinuse, thrombophilia, trauma

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91
Q

Locked in, vs coma, vs brain dead

A
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92
Q

What is transcortical motor and sensory aphasia

A

In true Broca and Wernicke aphasia, repetition is impaired. If repetition is intact, the deficit is called transcortical motor aphasia (TMA) or transcortical sensory aphasia (TSA), and it is caused by a lesion around either the Broca area or the Wernicke area, respectively. Also called secondary aphasia

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93
Q

Difference between transcorticle motor, sensory, wernicke, brocas,

A
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94
Q

episode of lip smacking associated with an impaired level of consciousness and followed by confusion, Dx?

A

think complex partial seizures.

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95
Q

If a patient presents with uncontrollable twitching of their thumb and is fully aware of their symptoms, Dx?

A

think simple partial seizures.

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96
Q

Labrytnhitiz vs vestibular neuritis

A

Labyrinthitis causes vertigo, Nystagmus and deafness. Where is vestibule neuritis doesnā€™t cause hearing problemsļæ¼

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97
Q

Lateral pontine/cerebellar stroke vs labrynthitis

A

Lateral pontine/cerebellar stroke (anterior inferior cerebellar artery territory) may present with similar symptoms but may have additional occipital headache, ataxia, nystagmus, and somatosensory deficits

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98
Q

Lateral medullary/cerebellar stroke vs vestibular neuritis

A

Lateral medullary/cerebellar stroke (posterior inferior cerebellar artery territory) can present with similar symptoms, but patients have focal findings on exam (ie, ataxia, sensory loss, dysphagia, Horner syndrome).

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99
Q

Complication regarding hearing in merniere (consider frequency)

A

Patients progressively lose low-frequency hearing over years and may become deaf on the affected side.

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100
Q

When the cause of AMS is not apparent after initial assessment, can we empiric treat for likely causes (eg, WE)

A

Yes

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101
Q

Pregnancy and post partumā€¦ are these risks or protective for MS Flare

A

pregnancy is protective for MS, but there is an increased risk in the early postpartum period.

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102
Q

When to do LP in MS. Recall Laith chat

A

If MRI or clinical is equivocal

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103
Q

Steroid dosing for PMR, GCA and GCA with vision loss

A

PMR only: low-dose oral glucocorticoids (eg,
prednisone 10-20 mg daily)

ā€¢ GCA: intermediate- to high-dose oral glucocorticoids (eg, prednisone 40-60 mg daily)

ā€¢ GCA with vision loss: pulse high-dose IV glucocorticoids (eg, methylprednisolone 1,000 mg
daily) for 3 days followed by intermediate- to high- dose oral glucocorticoids

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104
Q

How can fistula in dialysis cause ischemia to arm

A

The vascular steel. See on google

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105
Q

How does dialysis increase B microglob?

A

The inflam causes increased microglob, but the dialysis machine cannot remove it.

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106
Q

Uremic polyneuropathy is common in patients with ESRD, and causes what signs. Hands or feet more?

A

causes progressive pain and paresthesia in the feet, not the hands so much

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107
Q

Is the syphilis attack on the SC direct or indirect

A

Treponema pallium directly damages dorsal sensory roots
Secondary degeneration of the dorsal columns

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108
Q

Signs of cervical myelopathy (the whole axial atlanti subluxation thing

A

-Neck pain radiating to occipital region
-Slowly progressive spastic quadriparesis
-Painless sensory deficits in hands or feet
ā€¢ Respiratory dysfunction (eg, from vertebral artery compression)

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109
Q

What is Hoffman signs

A

Hoffman sign (flexion and adduction of the thumb when flicking the nail of the
middle finger) suggests a corticospinal tract lesion

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110
Q

Mx for atlantoaxial subluxation

A

Management involves stiff surgical collars and neurosurgical intervention

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111
Q

What is Critical illness polyneuropathy

A

complication of sepsis characterized by axonal injury of the peripheral nerves. It is a common cause of weakness after a prolonged stay in an intensive care unit.

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112
Q

Is stroke onset of symptoms usual gradual or sudden

A

stroke typically occurs acutely with maximum weakness upon presentation

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113
Q

Signs of transverse myelitis

A

motor and sensory loss below the level of the lesion with bowel and bladder dysfunction. Patients initially have flaccid paralysis (spinal shock), followed by spastic paralysis with hyperreflexia.

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114
Q

Main causes of traumatic carotid artery dissection

A

Penetrating trauma
ā€¢ Fall with object in mouth
(eg, toothbrush, pencil)
ā€¢ Neck manipulation (eg, yoga, sports)

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115
Q

Signs of traumatic carotid artery dissection

A

Gradual-onset hemiplegia
ā€¢ Aphasia
ā€¢ Neck pain
ā€¢ ā€œThunderclapā€ headache

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116
Q

Invx of choice for traumatic carotid artery dissection

A

CT or MR angiography

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117
Q
A

Chiari I

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118
Q

Symptoms sus for pseudotumour cerebri. Order what first

A

MRI is performed before lumbar puncture to exclude other
causes of elevated IP (eg, space-occupying mass) that would increase the risk of cerebral herniation

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119
Q

Bifrontal ,,migraines are more common in which patient demographic

A

Children

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120
Q

Does severe AS or other causes of cerebral low perfusion cause vertigo

A

NO. they cause light headdressā€¦.. not the same

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121
Q

Dx the vertigo

Recurrent episodes lasting 20 minutes to several hours
ā€¢ Sensorineural hearing loss
Tinnitus &/or feeling of fullness in the ear

A

merniere

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122
Q

Dx the vertigo

Brief episodes triggered by head movement
ā€¢ Dix-Hallpike maneuver causes nystagmus

A

BPPV

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123
Q

Dx the vertigo

ā€¢ Acute, single episode that can last days
Often follows viral syndrome
ā€¢ Abnormal head thrust test

A

Vestibular neuritis. Labyrinthitis if includes deafness

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124
Q

Cephalohematoma Mx

A

management is with observation. As blood from the cephalohematoma breaks down,
the patient is at increased risk for hyperbilirubinemia and may require phototherapy. cephalohematomas typically resorb spontaneously within a month,

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125
Q

Dx scalp swell

hours after birth with a firm, nontender, nonfluctuant scalp swelling. The swelling is well demarcated and confined to the surface of a single bone because the hematoma does not cross suture lines.

A

Cephalohematoma

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126
Q

Dx scalp swelling

diffuse, fluctuant scalp swelling that expands after delivery.

A

Subgaleal hemorrhage

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127
Q

In the prepubertal population pseudotumour cerebri is more headache or vision predominant

A

In the prepubertal population, headache may be less obvious and vision abnormalities may
be the predominant finding.

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128
Q

Dx this

Limited upward gaze
ā€¢ Upper eyelid retraction (Collier sign)
Pupillary abnormalities (ie, reactive to accommodation but not to light)

A

Parinaud syndrome

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129
Q

When pineal glands cause hydrocephalus, where do they obstruct

A

aqueduct of Sylvius,

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130
Q

What is a trilateral Rb

A

trilateral retinoblastoma consists of bilateral retinoblastoma and a pineal gland tumor.

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131
Q

We all know CNIII can be due to Post comm artery berry. What can cause CN IV or VI.

A

Less commonly, a trochlear (CN IV) or abducens (CN VI) nerve palsy can result from an aneurysm affecting the superior cerebellar or anterior inferior cerebellar artery, respectively.

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132
Q

Severe headache in the setting of CNIII lesion likely indicates what?

A

Berry aneurysm and SAH

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133
Q

Mx of SAH

A

Management of a patient with sudden-onset, severe headache should involve head CT scan with angiography to evaluate for active SAH or an enlarging aneurysm with impending rupture.

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134
Q

unilateral headache and ipsilateral Horner syndrome. Dx?

A

Carotid artery dissection typically

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135
Q

Cluster causes symptoms or parasympathetic signs

A

Parasymp

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136
Q

Preventions for migraines

A

Topiramate
ā€¢ Divalproex sodium
Tricyclic antidepressants
ā€¢ Beta blockers (eg, propranolol)

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137
Q

Abortive for migraines

A

Triptans (eg, sumatriptan)
ā€¢ NSAIDs (eg, naproxen)
ā€¢ Acetaminophen
ā€¢ Antiemetics (eg, metoclopramide, prochlorperazine)
ā€¢ Ergotamines (eg, dihydroergotamine)

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138
Q

Who gets propels for migraines

A

Have frequent (eg, >4/month) or long-lasting (eg, >12 hours) episodes
ā€¢ Experience disabling symptoms that prevent regular activities despite abortive treatment
ā€¢ Are unable to take or have had no relief with abortive medications
ā€¢ Overuse abortive medication (eg, nonsteroidal anti-inflammatory drugs (NSAIDs]) and have rebound
headache

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139
Q

When to do imaging for headache patients

A

Neurologic findings: Seizure, changes in consciousness, specific deficits
ā€¢ Differences compared to prior headaches: Change in frequency, intensity, characteristics
ā€¢ Other: New at age >40, sudden onset, trauma, present on awakening

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140
Q

If the neurologic examination is consistent with brain death, do what to confirm brain death

A

the patient can be removed from the ventilator for an apnea test. A positive apnea test confirms brain death by documenting an absent respiratory response

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141
Q
A
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142
Q

Concussion return to play

A
  • Remove from same-day physical play
    ā€¢ Neurologic evaluation
    ā€¢ Rest for ā‰„24 hr
    ā€¢ Gradual return to normal activity if symptoms do not worsen
    ā€¢ Physical: light aerobic exercise -ā€ŗ noncontact sports -ā€ŗ contact sports
    ā€¢ Neurocognitive: limited screen time, school accommodations (eg, frequent breaks
    shortened days)
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143
Q

Concussion pathogensis

A

Pathogenesis involves axonal shearing from rotational acceleration of the brain after a fall or strike to the head.

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144
Q

When to do neuroimaging in concussion

A

Neuroimaging is not required
for diagnosis but may be performed to exclude structural intracranial injury (eg, contusion, hematoma) in patients
with high-risk features (eg, vomiting, loss of consciousness).

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145
Q

What is second impact syndrome, in relation to concussion

A

recurrent head injury from any contact sport during the initial recovery
period can lead to second impact syndrome, which is characterized by cerebral edema and can be fatal.

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146
Q

severe traumatic brain injury. Initial head CT scan was unremarkable (eg, no large
hematoma), this presentation is most consistent for what?

A

diffuse axonal injury (DAI).

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147
Q

Features of benign macroceph. Mx?

A

Head circumference in 98% percentile And
ā€¢ Normal development
ā€¢ No syndromic features
ā€¢ No signs of increased intracranial pressure (eg, bulging fontanelle)
ā€¢ No signs of infection (eg, fever, lethargy)

Reassure that babaaayyyy

148
Q

Dx of status E (time wise)

A

ā€¢ 5 minutes of generalized convulsive seizure
OR
ā€¢ 2 generalized convulsive seizures without interval recovery of
consciousness

149
Q

Mx of status E

A

Stabilize circulation, airway & breathing
ā€¢ Benzodiazepines (repeat administration until termination of seizure
activity)
ā€¢ Begin antiepileptic drugs like Leve
ā€¢ EEG monitoring for refractory status epileptics or failure to regain
consciousness

150
Q

Persistent
unresponsive state, after status E may be due to either:
ā€¢ Sedation due to persistent effects of benzodiazepines or
ā€¢ ongoing seizure activity without physical manifestations (ie, nonconvulsive status epilepticus).
How to DDx the two?

A

electroencephalography should be performed.

151
Q

Did a lil too much benzos for seizing patient. Patient a lil drowsy. Do we flumanezil them?

A

because of the risk of precipitating
further seizures, sedation related to benzodiazepine use after status is managed with supportive therapy (eg,
securing airway and assisting breathing if necessary) rather than flumazenil.

152
Q
A

Appreciate this! Big deal

153
Q

Restless leg syndrome causes

A

Iron deficiency anemia
ā€¢ Uremia (ESRD, CKD)
ā€¢ Diabetes mellitus
ā€¢ Multiple sclerosis, Parkinson disease
ā€¢ Pregnancy
ā€¢ Drugs (eg, antidepressants, metoclopramide)

154
Q

Pharma two. Drugs for restless leg syndrome

A

Pramipexole (DA ag), gabapentin. Fe if the cause is iron def

155
Q

Gabapentin MOA

A

Gabapenti, has an effect on GABA activity but does not directly target GABA receptors. Actually blocks calcium receptor channels

156
Q

Tx of malignant hyperthermia

A

Respiratory/ventilatory support
cessation of causative anesthetic
ā€¢ Dantrolene

157
Q

Neuroleptic malignant syndrome vs malignant hyperthermia. Which is more acute onset

A

Malig hyperthermiaā€¦ usually over minutes.

158
Q

Chronic inflammatory demyelinating polyneuropathy

Pathophysiology
Clinical findings
Dx
Tx

A

Pathophysiology
ā€¢ Immune-mediated demyelination of peripheral nerves and nerve roots
ā€¢ Non-length dependent

Clinical features
ā€¢ Progression >8 weeks
ā€¢ Motor&raquo_space; sensory
ā€¢ Symmetric proximal & distal muscle weakness
ā€¢ LMN signs (eg, hyporeflexia, atrophy)

Glucocorticoids
Intravenous immunoglobulin
Plasmapheresis

Dx
CSF: 1 protein, normal white blood cells
ā€¢ NCS: decreased conduction velocity (ie, demyelination)
ā€¢ Nerve biopsy: segmental demyelination

159
Q

Likely Dx

both proximal (eg, standing up) and distal (eg, buttoning
shirts) muscles weakened, accompanied by lower motor neuron signs (eg, hyporeflexia, muscle atrophy) and sensation deficits (more motor though). Developed over 10 weeks

A

Chronic inflam demyelinating polyneurp
In contrast to many other polyneuropathies (eg, diabetic), CIDP is not length dependent. Therefore, it classically causes both proximal (eg, hip girdle) and distal (g, hand) muscle weakness. Symptoms develop over >8 weeks.

160
Q

CK and ESR levels in
GC myopathy
Myosotis
PMR
HYPOTHYROIDISM MYOPATHY
statin myopathy

A

GC myopathy Normal, normal
Myositis high, high
PMR normal, high
HYPOTHYROIDISM MYOPATHY high, normal
statin myopathy high, normal

161
Q

NF2, three things to surveillance

A

Audiogram
Ophthalmologic evaluation
ā€¢ MRI of the brain & spine

162
Q

What is medication overuse headache

A
163
Q

Why do patients generally not get vertigo in schwannoma

A

Most patients
do not experience vertigo because the tumorā€™s slow growth allows for central compensation of gradual loss of
input.

164
Q

Dx?

Bilateral motor weakness, classically early flaccid (LMN) progressing to late spastic
(UMN)
Bilateral sensory dysfunction (all somatosensory systems)
Distinct sensory level
ā€¢ Autonomic dysfunction (bowel &/or bladder)

A

Transvers myelitis

165
Q

Transverse myelitis vs B12 def timing of symptoms

A

Acute and not acute resp

166
Q

Tx of vasovagal syncope

A

Reassurance & avoidance of triggers
ā€¢ Counterpressure techniques for recurrent episodes

167
Q

Brain finding in status Ep

A

a brain that has seized for >5 minutes is at increased risk of
developing permanent injury due to excitatory cytotoxicity.
Cortical laminar necrosis is the hallmark of prolonged seizures and can lead to persistent neurologic deficits and recurrent seizures.

168
Q

MG risk factors (mainly meds)

A

Medications: antibiotics (eg,
fluoroquinolones, aminoglycosides),
neuromuscular blocking agents, cardiac
medications (eg, BBs), MgSOA,
penicillamine
ā€¢ Physiologic stress: pregnancy/childbirth,
surgery (especially thymectomy), infection

169
Q

Tx for MG

A

AChE inhibitors (eg, pyridostigmine) ā€”
immunotherapy (eg, corticosteroids,
azathioprine)
ā€¢ Thymectomy

170
Q

Patients with MG who remain symptomatic despite pyridostigmine therapy generally require

A

chronic immunosuppressive therapy (eg, corticosteroids, azathioprine), which may induce remission but generally
takes weeks to reach clinical efficacy.

171
Q

Essential tremor treatment is propranolol, but whatā€™s the second line

A

Primadone

172
Q

What is neuropathic tremor,where is it seen

A

Neuropathic tremor occurs with large-fiber neuropathies (eg, chronic inflammatory demyelinating
polyneuropathy). Although it is also an action tremor that predominantly affects the distal extremities, patients with
neuropathic tremors often show other signs or symptoms of peripheral neuropathy (eg, proprioceptive or sensory
loss, weakness).

173
Q

Fist invx and Dxic Invx for galactosemia

A

Supportive laboratory findings on presentation include nonglucose urine reducing
substances suggestive of galactosuria. Absent GALT activity in red blood cells confirms the diagnosis.

174
Q

Dx this

30 wk gest premat
Seizures or apnea
ā€¢ Full fontanelle
Acute anemia

A

Intraventricular hemorrhage

175
Q

Premat screening for which thing?

A

Head US for Intraventricular hem
Any <32 week gest

No screening for NEC or PDA (abd us or echo resp)

176
Q

Intracerebral hem common locations

A

basal ganglia (putamen), cerebellar nuclei, thalamus, pons, and cerebral cortex. In order

177
Q

Gradual onset of symptoms vs acute onset. Which is hemorrhagic and which is Ischemic

A

Ischemic is acute onset, hemorrhagic is gradual over hiurs

178
Q

Signs of cerebellar hemorrhageā€¦ explain reasoning behind each sign

A

occipital headache (may radiate to neck/shoulders), neck stiffness (due to extension of blood into the 4th ventricle), nausea/vomiting, and nystagmus. Patients may also have ipsilateral hemiataxia of the trunk (cerebellar vermis) and/or limbs (cerebellar hemispheres)

179
Q

Worsening limb pain and paresthesia in response to lateral neck flexion is relatively specific for

A

cervical radiculopathy,

180
Q

Acute intermittent porphyriaā€¦.. neuropathy usually where?ā€¦

A

Peripheral neuropathy most pronounced in the
proximal upper extremities

181
Q

Can we see autominc signs in acute intermittent porphyria

A

Yes ā€¢ Autonomic dysfunction (eg, tachycardia,
diaphoresis, hypertension)

182
Q

Tx for AIP

A

Glucose & hemin (heme analogue)

183
Q

Name some weird findings seen in acute intermittent porphyria

A

SIADH, ans dysfunction, urobilingen high,

184
Q

Please mention the signs of Lesch Nyhan. Including the neuro stuff

A

Delayed milestones & hypotonia in infancy
ā€¢ Early childhood
ā€¢ Intellectual disability
ā€¢ Extrapyramidal symptoms (eg, dystonia,
chorea)
ā€¢ Pyramidal symptoms (eg, spasticity,
hyperreflexia)
ā€¢ Self-mutilation
ā€¢ Gouty arthritis in late, untreated disease

185
Q

Which area of the brain is most affected in Lesch Nyhan

A

Dopaminergic areas. So movement issues ensue, alongside behavioural issues. Then obvs the unic acid stuff

186
Q

Levels of what can be used to DD. seizure for, pseudo seizure

A

Serum prolactin levels, which are usually elevated immediately following seizure, are used primarily to
differentiate seizure from pseudoseizure (psychogenic nonepileptic seizure) in adults;

187
Q

Localising signs after seizure (esp in kids) DDx? And what to do to tell

A

Toddā€™s paralysis and stroke,,,, so need MRI to tell

188
Q

Miller Fischer recap

A

Anti-GQ1b antibodies re
characteristic symptoms of MFS include cerebellar-like ataxia (eg, dysmetria) and areflexia and opthalomoplegia and weakness.

189
Q

Botulism toxicity

A

is associated with a symmetric descending weakness ophthalmoplegia may occur, facial
weakness, dysphagia, and dysarthria are typical.

190
Q

Pathophysiology of syndemans chorea

A

Molecular mimicry between anti-GAS antibodies & neuronal antigens in basal ganglia

191
Q

Symptoms of syndemans chorea

A
  • Involuntary, jerky movements (worse while awake & with action)
    ā€¢ Hypotonia
    ā€¢ Emotional lability, obsessive-compulsive behaviors
    ā€¢ ā€” Symptoms of acute rheumatic fever
192
Q

Tx of syndemans chorea

A

ā€¢ Chronic antibiotics (eg, penicillin G)
ā€¢ Symptomatic (antidopaminergics [eg, haloperidol])

193
Q

Does the abnormal movement in chorea continue in sleep?

A

patientā€™s abnormal, jerky movements that disappear during sleep are consistent with chorea,

194
Q

First line therapy for
myoclonus;

A

GABA agonist medication clonazepam (a benzodiazepine) is a first-line treatment

195
Q

AVM signs and symptoms

A

recurrent headache, seizure, or focal neurologic deficit (due to compression).if burst can cause SAH or ICH

196
Q

Mx of FT lobe dementia

A

No cure, but can give SSRI or atypical antipsychotic for symptoms

197
Q

How to maintain CPP in TBI. Consider both components

A

Maintain MAP: isotonic fluids, vasopressor therapy
ā€¢ Reduce ICP: head elevation, sedation, osmotic therapy (eg, hypertonic saline,
(= MAP - ICP)
mannitol), decompressive interventions (eg, SF removal, craniectomy)

198
Q

How to prevent ICH in TBI. One Med we give

A

ā€¢ Antifibrinolytic therapy (ie, tranexamic acid) within first 3 hr. Prevents the local DIC-like reaction (-Kyle)

ā€¢ Reversal of preexisting anticoagulation

199
Q

How to prevent seizure in TBI. Target glucose and BPā€¦ how to achieve?

A

Prevent seizures (eg, levetiracetam, phenytoin)
ā€¢ Control blood glucose (eg, insulin to target 140-180 mg/dL glucose)
ā€¢ Maintain normothermia (eg, antipyretics, surface-cooling devices)

200
Q

Signs of Alzheimerā€™s at the beginning

A

ā€¢ Anterograde memory loss (ie, immediate recall affected, distant memories preserved)
ā€¢ Visuospatial deficits (eg, lost in own neighborhood)
ā€¢ Language difficulties (eg, difficulty finding words)
ā€¢ Cognitive impairment with progressive decline

201
Q

Vascular dementia vs alz starting symptoms. In simple terms

A

More excec dysfunction in vascular. More memory in alz

202
Q

Invx for TG neuralgia

A

MRI/MRA. Conduction studies if cannot do MRI

203
Q

Why do TMJ disorder patients have morning headaches

A

Bruxism

204
Q

4 As of psychoneuro signs of fragile X

A

ADHD, autism, anxiety, auto canabal (Kyle)

205
Q

Why is OCP CI in migraine with aura..

A

These patients are at high risk of Ischemic stroke, so to reduce compound risk, must discontinue OCP

206
Q

Acute/subacute Herpetic neuralgia Mx

A

NSAIDs, analgesics

207
Q

Chronic post Herpetic neuralgia Mx

A

GabaP, or TCA, or pregabalin

208
Q

Difference between chorea and athetosis

A

Athetosis is a slow writhing. Whereas chorea is non rhythmic, brief irregular, unintentional contractions.

209
Q

Oscillopsia

A

Feeling of objects moving

210
Q

Positive head thrust testā€¦. Is peripheral or central vertigo

A

Peripheral

211
Q

Can CVD risk factor Management decrease the likelihood of alz

A

Yes, aggressive Mx in midife

212
Q

Most common psycho issues in Parkinsonā€™s

A

MDD (up to 20%)

213
Q

Dementia with Lewy body vs Parkinsonā€™s disease dementia

A

Parkinsonā€™s disease dementia , Parkinsonā€™s comes first by at least 1 year

214
Q

Parkinsonā€™s disease dementia Tx for halluc and Tx for dementia elements

A

Donepizil - dementia

Low dose antipsychotic - halluc

215
Q

Confusion assessment method for Delerium recquire?

A

Acute and fluctuating
Inattention
Disorganised thinking or altered consciousness

216
Q

Patients with Delerium are at increased risk of what, long term?

A

Cognitive decline

217
Q

Tx for lambert Eaton. And if that fails

A

Guanidine. IVIg/CS if refractory

218
Q

Main invx in sturg weber. The. Some Tx options

A

Do MRI. laser Tx for port wine stain. Anti epileptic maybe. Check IOP and make sure to keep it normal.

219
Q

Dx this:

Prolonged (>4 weeks) concussion symptoms after mild TBI:
ā€¢ Headache
ā€¢ Dizziness
Clinical features
o Sleep disturbance
o Mood changes
ā€¢ Cognitive impairment
ā€¢ No structural intracranial injury

A

Post concussion syndrome

220
Q

Orthostatic tremor

A

postural tremor considered to be a variant of essential tremor. Orthostatic
tremor occurs in the legs immediately on standing and is relieved by sitting down.

221
Q

Tremor predominant Parkinsonā€™s. Mx? If young or old

A

Anti cholinergic, or can do amantadine in older patients to avoid antiCh

222
Q

MAOI used in what Parkinsonā€™s

A

Mild conditions

223
Q

DA agonists ok in young or older patients for Parkinsonā€™s

A

Younger. Not well tolerated in older

224
Q

Screening for TS patients (just think of complications and youā€™ll know)

A

ā€¢ Tumor screening
ā€¢ Regular skin & eye examinations
ā€¢ Serial MRI of the brain & kidney
ā€¢ Baseline echocardiography & serial ECG
ā€¢ Baseline electroencephalography
ā€¢ Neuropsychiatric screening

225
Q

What is the growth pattern of a cardiac rhabdomyoma

A

Big in infancy, but regularly regresses itself

226
Q

List the following in order of most likely to met to the brain. Which two are the multiple nodule causing, and which other causing solitary nodules usually.

Breast
RCC
melanoma
Lung
Colon

A

Lung, boob, melanoma, colon, rcc

  • = multiple
227
Q

How would imaging be described for neurocysterocosis

A

Non enhancing, hypodense lesion, calcified granuloma

228
Q

Mumps triad of symptoms (doesnā€™t all occur)

A

Meningitis, orchitis , parotitis

229
Q

When is CT C. Spine imaging needed in traumatic injury

A

cervical spine imaging
ā€¢ Neurologic deficit
ā€¢ Spinal tenderness
ā€¢ Altered mental status
ā€¢ Intoxication
ā€¢ Distracting injury

230
Q

Best imaging modality for cervical spine

A

CT!! Not X-ray

231
Q

The presence of a single vertebral fracture in a patient with blunt trauma is an indication to image what.?

A

the entire spine. CT scan is the screening modality of choice. ~20% have concomitant fracture elsewhere

232
Q

How does Cervicle myelopathy cause upper and lower motor neurone symptoms

A

Cervical myelopathy often causes both spinal cord and spinal nerve root compression, resulting in myelopathic symptoms (eg, upper motor neuron signs below the lesion) and radicular symptoms (eg, lower motor neuron signs, pain in a dermatomal/myotomal pattern). Lhermitte sign (electric shock-like pain with neck flexion) may occur.

233
Q

Why can face infx cause cavernous sinus thrombosis easily

A

Because the facial/ophthalmic venous system is valveless, uncontrolled infection of the skin, sinuses, and orbit can spread to the cavernous sinus. Inflammation of the cavernous sinus subsequently results in life-threatening CST and intracranial hypertension.

234
Q

Unilateral and rapidly becoming BILATERAL CN (3,4,6) signs and headacheā€¦. Suggestive of what?

A

Cavernous sinus thrombosis

235
Q

Why does edema of the facial area occur in cavernous sinus thrombosis

A

Veins backlogs and cause hydrostatic edema

236
Q

New born vs adult botulinum Tx

A

Newborn= human Ig

Adult= equine anti toxin

237
Q

Does werdnig Hoffman affect the pupils?

A

No

238
Q

Adult botulinum has what prodrome that infant type doesnā€™t have

A

Has nausea and vom prior, and diarrhea

239
Q

Signs to differentiate seizure from orthostaiss

A

Seizure: post ictal state, auras, tongue bite, incontinence etc.

Orthostasis: rapid return to baseline, preceding light head, pallor or signs of vol depletion

240
Q

S1 radiculopathy overview

A

Posterior calf sense gone

ā€¢ Achilles reflex goes
ā€¢ Sole & lateral foot sense gone
ā€¢ Hip extension (gluteus maximus)
ā€¢ Foot plantarflexion (gastrocnemius)

241
Q

Muscles and weakness in L5 radiculopathy

A
  • Foot dorsiflexion & inversion (tibialis anterior)
    ā€¢ Foot eversion (peroneus)
    ā€¢ Toe extension (extensor hallucis and digitorum)
242
Q

Muscles weakened in L2-L4 radiculopathy

A

ā€¢ Hip flexion (iliopsoas)
ā€¢ Hip adduction
ā€¢ Knee extension (quadriceps)

243
Q

Which nerve root radiculopathy causes sexual dysfunction and incontinence

A

S2-24

244
Q

LP in the setting of potential epidural abcess?.

A

NO! Can seed into CNS. So do MRI prior

245
Q

Pseudobulbar vs bulbar palsy. Which is LMN and which is UMN

A

Bulbar is LMN. Pseudo bulbar is UMN

246
Q

Thalamus blood supply. Details

A

PCA and the thalamogeniculate branches

247
Q

Globes pallidus and hippocampus get the blood supply from which unusual artery

A

Anterior choroidal

248
Q

Tx for child mengitis (bacterial and above 1yo)

A

Vanco, ceph and dexameth (covers strep and neisseria)

249
Q

Why do we have to do audiological testing after paed bacterial meningitis

A

Cochlear damage is common. Therefore, because hearing deficits may go unrecognized, all patients with bacterial meningitis should undergo audiologic testing as soon as possible (ideally, before hospital discharge). If left to calcify, cochlear implants are hard to do

250
Q

Are brain abscess a long term or short term complication of meningitis

A

Short termā€¦. And not common after strep pneumoniae

251
Q

What are the subtypes of vascular dementia

A

Early, prominent executive dysfunction in most

Subtypes:
ā€¢ Multi-infarct: often with stepwise decline
ā€¢ Strategic infarct: associated with localizing cortical deficits (seen often with a noticeable stroke)
ā€¢ Subcortical vascular encephalopathy: associated with subcortical signs (eg, urinary
incontinence, gait disturbances)

252
Q

Difference between strategic infant vascular dementia, and multi infarct vascular dementia

A

Single, strategic infarction: One infarction may be enough to cause poststroke vascular cognitive
impairment if it affects key brain areas (ie, frontal lobes, thalamus).

ā€¢ Multiple infarctions: Multi-infarct dementia occurs when small infarcts combine to cause enough cumulative damage to the brain, resulting in noticeable cognitive deficits. Patients may not have a history of overt stroke but rather have a stepwise decline in cognitive function.

253
Q

CZDā€¦ incub period?

A

Can be up to 10 years. Obvs once symptoms starts, will kill you in a year

254
Q

Tx for CZD

A

Symptomatic treatment only. Nothing to do to slow progresion

255
Q

Mx overview for pseudotumour cerebri

A

carbonic anhydrase inhibitors
first-line treatment for idiopathic intracranial hypertension
medication

a loop diuretic can also be added as adjunctive therapy to decreases the rate of CSF production

Operative
optic nerve sheath fenestration
in patients who fail medical management

256
Q

Mx non pharma for Delerium

A

Environment:
noise reduction, intervention grouping
ā€¢ Sleep facilitation: bright day/dim night lighting

ā€¢ Personal interaction: reassurance, physical touch
ā€¢ Constant observation: family, professional sitters
ā€¢ Mobilization: out of bed, restraint avoidance

257
Q

Pharma Mx for Delerium

A
  • Pain management: nonopioid when possible
    ā€¢ Antipsychotics: off-label indication
    ā€¢ Benzodiazepines: antipsychotic failure/withdrawal syndromes
258
Q

Why do pyramidal defects cause pronator drift

A

UMN lesions cause more weakness in supinators > pronators.

259
Q

Mx of hospital Delerium

A

Reduce noise, improve room lighting, open window blinds during the day & avoid frequent room changes
ā€¢ Constant observation by a familiar person at the bedside, preferably a family member
ā€¢ Nonpharmacologic sleep aids for insomnia
ā€¢ Early mobilization & minimal use of physical restraints
ā€¢ Visual & hearing aids when appropriate
ā€¢ Early volume repletion for dehydrated patients
ā€¢ Adequate pain control
ā€¢ Aggressive chronic disease management (eg, diabetes, COPD)
ā€¢ Reduce polypharmacy
ā€¢ Monitor & treat for metabolic disturbances, infections & drug toxicity

260
Q

Likely Dx

progressive ascending paralysis over hours. more pronounced in 1 leg or arm,t. Fever is not present. Sensation is normal. There is no autonomic dysfunction. CSF normal.

A

Tick induced paralysis

Remove tick and symptoms should improve

261
Q

Describe the LMN UMN change in anterior SC syndrome

A

Spine shock, means itā€™s LMN deficit first, then within days it becomes UMN. We obvs have loss of crude touch, pain, temp too.

262
Q

Explain the cause and presentation of central cord syndrome

A

Caused usually by hyperextension of neck in Cervicle spondylosis. See image to explain presentation

263
Q

CNS infections key words:
Photophobia, nuchal rigidity =
Focal neurologic deficits =
Confusion, altered mental status =

A

CNS infections key words:
Photophobia, nuchal rigidity = meningitis
Focal neurologic deficits = brain abscess
Confusion, altered mental status = encephalitis

264
Q

We know the three ways people can get brain abcess. Anatomical where do abscesses that form from blood spread form

A

At gray white matter boundaries.

265
Q

We know the three ways people can get brain abcess. Anatomical where do abscesses that form from blood spread form

A

At gray white matter boundaries.

266
Q

Classic triad for brain abcess

A

Fever, headache and focal neuro

267
Q

Describe the age sex epidemiology of M.G.

A

Age sex dependent. In young women and old men

268
Q

Meds causing or worsening myasthenic crisis

A

antibiotics (aminoglycosides recall NMJ tox, fluoroquinolones), hydroxychloroquine, and Ī²-blockers can precipitate crisis

269
Q

Main way to tell MG vs antimuscarinc tox?

A

AntiM will have ANSā€¦. MG crisis wont

270
Q

Examples of ANS dysfunction in LES

A

This results in autonomic dysfunction, including xerostomia, erectile dysfunction, constipation, and impaired pupillary light response.

271
Q

HLA loci in MS

A

MS has been associated with the HLA-DRB1 locus

272
Q

Which MS type has the best Px

A

Those with a relapsing and
remitting history have the best prognosis.

273
Q

How to enhance active MS lesions on MRI

A

Active lesions are enhanced with gadolinium.

274
Q

Miller Fischer triad AAA

A

ophthAlmoplegia, Ataxia, and Absent reflexes.

275
Q

Significance of hyponatremia in GBS

A

hyponatremia can occur and is a poor Px indicator

276
Q

Remember that ascending paralysis with normal CSF findings and without autonomic dysfunction is characteristic of tick-borne paralysis, not Guillain-BarrƩ syndrome.

A

STATEMENT IN FIRST AID YOU TIT

277
Q

MMSE score from mild to major cognitive disorder

A

24-27 mild. Less than 24 is major

278
Q

DUM MUD for Alzheimerā€™s and NPH

A

Alzheimer (DUM): Dementia (early, short-term memory) > Urinary incontinence > Motor

NPH (MUD): Motor (early, gait ataxia) > Urinary incontinence > Dementia

279
Q

Difference between Parkinsonā€™s gate and normal pressure hydrocephalus gate

A

Normal pressure hydrocephalus has preserved arm swinging. Also will not have any tremor

280
Q

First signs of normal pressure Hydrocephalos

A

Magnetic gate

281
Q

What are the good and bad prognostic indicators in normal pressure hydrocephalus

A

Only motor problems is good, presence of even a mild dementia is

282
Q

What is the hockey stick sign and which disease is it seen in

A

It is hyperintensity of the caudate in the puteman , seen in Creutzfeldt Jakob

283
Q

Pathophys of Huntingtonā€™s

A

excessive trinucleotide (CAG) repeats on chromosome 4 during spermatogenesis ā†’ abnormally long huntingtin protein ā†’ glutamate excitotoxicity via the NMDA-Rā†’ degeneration of cerebrum + striatum (caudate + putamen) ā†’ loss of gamma-aminobutyric acid (GABA)/ACh, unbalanced dopamine (DA) activity ā†’ triad of motor (chorea), memory (executive dysfunction), and mood (irritability) symptoms.

284
Q

Restlessness and fidgetiness. Delete the cards. This could be a presentation of an early phase of what movement disorderļæ¼

A

Huntingtons disease, donā€™t make my mistake

285
Q

Pattern of movement issues in Huntingtons disease. Consider early in the disease and late on

A

Earlier on I have coria, hyperreflexia, urge incontinence. Later on in the disease they become hypokinetic, rigid,, dystonic, dysphasia et cetera

286
Q

What are some of the pre-clinical Parkinsonā€™s symptoms

A

Constipation, anosmia, sleep disturbance (rem disorder, restless leg, excess sleepiness) and mood disorders like depression and anxiety. Can pre-date by up to 20 years

287
Q

Name the loss of neurones/neurotransmitters in each of the following, and the cardinal symptom. Parkinsonā€™s, Alzheimerā€™s, ALS, myasthenia gravis, Huntingtonā€™s

A

Parkinsonā€™s: loss of doper neurons in the basal ganglia causing extra pyradimal motor symptoms ļæ¼

Alzheimerā€™s disease: loss of cholinergic neurons in the cortex and subcortex causing dementia.

ALS: loss of upper and lower motor neurones.

My senior gravis: loss of acetylcholine receptor function, causing fatigability

Huntingtons disease: loss of Gabba and acetylcholine activity in the cerebrum and straighten. Causing unbalance dopa activity, causing Moto memory and mood signsļæ¼

288
Q

A couple of things that can help you differentiate ALS from a cervical myelopathy

A

Symptoms can be similar (UMN and LMN) Generally ALS will have no bladder disturbance and has a normal cervical MRI. Any involvement of cranial nerve tongue or a pharynx suggests pathology above the foreman magnum and this ALS rather than cervicalļæ¼

289
Q

What is pseudobulbar affect

A

Honestly what you have. Crying in somewhat sad moments and excessively laughing in mildly amusing moments. Can be seen in any CNS condition, like MS, ALS, Stroke et cetera

290
Q

What is postural tremor. Versus kinetic tremor

A

Tremor of hand only when lifted against gravity. Kinetic Tremor is tremble with any voluntary movement

291
Q

When is postural tremor seen? When is kinetic tremor seen?

A

Postural scene in physiological tremor and essential tremor

Kinetic is seen in intention tremor and essential tremor

292
Q

Wilsonā€™s disease main renal complication

A

Fanconi

293
Q

MRI findings of VHL

A

IC calcifications resembling tramline

294
Q

Sturgeon Weber MRI findings

A

IC calcifications resembling a tramline

295
Q

VHL type 1 and 2. Which has risk for phea

A

Type II

296
Q

Phae in less than 18 yo. High chance of what?

A

VHL

297
Q

Apart from HARP, what else do we see in VHL

A

Cyst adenoma of pancreas, endolymphatic sac tumour, epididymis cyst

298
Q

Ataxia telangiectasia

A

Autosomal recessive disease caused by a mutation in the ATM gene, which encodes DNA repair enzymes. Leads to aberrant repair of double-stranded DNA breaks, causing cell death (eg, Purkinje cells in the cerebellum are particularly susceptible).

Cerebellar ataxia is often the first presenting symptom in infancy or early childhood. Patients may also present with ocular apraxia (inability to control purposeful eye movements), cognitive impairment, extrapyramidal symptoms, and peripheral neuropathy.
Telangiectasias are common, most often in the face, eyes, and ears.
Immune deficiency (especially IgA) predisposes patients to recurrent sinopulmonary
infections, which may lead to interstitial lung disease.

Up to one fourth of patients will develop a malignancy, most often lymphomas or leukemias.

299
Q

Orthostasis blood pressure defined as?

A

SBP drop of >20! DBP >10

300
Q

Tandem gait testing is what?

A

Heel toe walking

301
Q

Eye findings in huntingtons

A

Delayed saccades

302
Q

Main cognitive impairment domain in HTT

A

Excec function

303
Q

Pathophysiology of epidural local anaesthetic systemic toxicity. What are the signs and symptoms

A

Essentially the needle can release local anaesthetic directly into the epidural vasculature. This will cause inhibition mainly of inhibitory pathways, which causes nerve over stimulation. Patients get perioral numbness, tinnitus, metallic taste in mouth, high blood pressure, tachycardia, and potentially cardiovascular collapse

304
Q

Describe some of the symptoms of oxytocin toxicity, and the reason behind them

A

Oxytocin shares similar structure to ADH, causing low sodium, Thos cerebral oedema, seizure

305
Q

What respiratory changes are seen in Rett syndrome

A

Tachypnoea and times of low/absent respiratory rate. Due to medullary centre neurones regressing

306
Q

Abulia

A

Lack of Will or initiation

307
Q

Apraxia

A

Inability to carry out complex motions

308
Q

Name a couple of signs that you would see in an anterior cerebral artery stroke

A

Abulia, apraxia, primitive reflexes, emotional disturbance, executive function, flat affect, bladder problems, leg weakness and sensory loss

309
Q

Clumsy hand syndrome as seen in which kind of stroke

A

Lacuna

310
Q

Infant has microcephally, whatā€™s the first thing that you should do. In the case That all of the growth is normal and the patient a stable and developing ok

A

Measure parents head circumference to assess for family or microcephally. ļæ¼

311
Q

Tell me some clues that can help differentiate cervical myelopathy from cervical radiculopathy

A

Myeloprhy is going to cause spinal cord compression. So will cause maybe a few radiculopathy signs, plus upper motor neuron signs, and lower extremity weakness, which is bilateral. Radiculopathy just will cause one side, lower motor neuron, following dermatome patterns usuallyļæ¼

312
Q

Vertebral body squaring is an early sign of what disease

A

Ankylosing spondylitis

313
Q

Symptoms of central venous thrombosis. Dx and Mx?

A

Headache, ICP signs, seizure sometimes. Can do MRV to Dx. Do anticoag

314
Q

What kind of stroke can cause unilateral MLF lesion

A

Pontine from lacunae stroke

315
Q

Difference between lateral geniculate nucleus and edinger Westphal

A

Edinger westphal is in the light reflex pathway, whereas LGN is in the normal optic pathway

316
Q

Medial Lemniscus lesion

A

Contra loss of vibr proprio and light touch

317
Q

Signs of post concussion syndrome

A

Noisy sensitivity, cognitive impairment, dizziness, headache, anxiety, irritability

318
Q

Most common cause of central cord syndrome

A

Whiplash type injury (hyperextension of the neck) in an elderly patient with cervical spondylosis.

319
Q

Signs and symptoms of central called syndrome

A

That usually happens in the cervical region: upper extremity motor, sensory loss bilaterally. Usually loss of reflexes due to anterior horn involvement. Lower extremities usually spared (recall anatomy of spinal cord)

320
Q

If you see muscle weakness in almost all the muscles of the body, and maybe a little bit of pain. What should be on your suspicion

A

An electrolyte problem

321
Q

List causes of enhanced physiological tremor

A

Medication such as beta agonists, SSRI, TCA, nicotine, caffeine, steroids. Stress and anxiety. Hypoglycaemia, alcohol/opioid withdrawal, thyrotoxicosis and liver disease

322
Q

Name all the signs of basil a skull fractures

A

Raccoon eyes, CSF rhinorrhoea CSF otorhea, postauricular Ekhymosis (a.k.a. Battle sign)

323
Q

Which neonatal scalp swelling is soft, and boggy and crosses suture lines. But is not life-threatening

A

Caput succedaneum ļæ¼

324
Q

Which neonatal scalp swelling is this: present after birth, is firm and non-fluctuant. Does not cross suture lines. Patient is okay. And what is the prognosis

A

Prognosis is good but there is a hyperbilirubinaemia risk. This is cephalo haematomaļæ¼

325
Q

Which neonatal scalp swelling is this. Diffuse soft fluctuant expansion over days. Crosses suture line. Can have a bit of bruising overlying it. Patient is someone un stable

A

Subgaleal haemorrhageļæ¼

326
Q

Main timing aspect to differential between plagiocephally and neonatal scalp swelling

A

Neonatal scalp swelling is in neonates. Plagiocephaly is in young infantsļæ¼

327
Q

Risk factors for sudden infant death syndrome

A

Maternal substance use, not only is less than 20, inconsistent prenatal care, prematurity or low-birth-weight, prone sleeping position, soft sleep surface, loose bedding, bed sharing, exposure

328
Q

NMS the lumbar puncture siesta will have high or normal total protein? And high or normal proportion of Ig to rest of protein

A

Normal total protein, but high immunoglobulin proportion

329
Q

Investigation of choice for Hydrocephalus in children

A

CT or MRI. Ultrasound is not as details, and does require a very wide fontanelle to investigate

330
Q

ļæ¼ Bellā€™s palsy, trigeminal neuralgia. Which is characterised by demyelination/atrophy, and which is characterised by inflammation/oedema

A

Trigeminal neuralgia is characterised bye demyelination and atrophy. Is Bellā€™s palsy is characterised by oedema/inflammationļæ¼

331
Q

Wardenburg syndrome, structures affected and subsequent symptoms

A

Spinothalamic tract, causing sensory loss Contralaterally. Vestibular nuclei causing usual signs. Furious cerebellar peduncle causing ataxia. Nucleus ambiguous causing dysphasia and dysphonia. Trigeminal nuclei causing loss of face at sensationļæ¼

332
Q

Dissection of the vertebral artery is commonly caused by what kind of trauma?

A

Rapid expansion of the neck

333
Q

Intracranial vertebral artery dissection can affect which important arteries

A

The posterior inferior cerebellar artery, causing Wallenberg syndrome

334
Q

Only mandatory sign for diagnostics of normal pressure hydrocephalus

A

Gait.ļæ¼ Incontinent and dementia are not required

335
Q

Can pseudodementia have an MCA score of the 27

A

Yes

336
Q

List some of the neurological complications of sarcoidosis

A

Cranial nerves! Especially facial nerve palsy. Central diabetes insipidus and other hypogonadotropic hypogonadism.

337
Q

Does cryptococcal meningitis CSF have normal or low glucose

A

Low, usually

338
Q

Likely diagnosis of this. Patient had no headaches for a long time, worse in the morning. Now starting to get weakness on the left side. Cardiovascular risk factors of moderate

A

Intracranial tumour.

339
Q

The signs and symptoms of decompression sickness

A

Respiratory distress, confusion, mottled skin, signs of stroke, especially tingling sensations. Obstructive shock can occur if large coalesced airļæ¼

340
Q

What is the tetrad for gerstmann syndrome. Where is the lesion

A

Finger agnosia, right left discrimination, acalculia, Agraphia (writing by hand). This is a lesion on the angular gyrus of the dominant hemisphereļæ¼

341
Q

Symptoms of lesions in the non-dominant parietal lobe

A

Heavy neglect, distortion of position sense (feelings of floating) and interpretation of objects (i.e. sighs)

342
Q

How does facet dislocation present

A

A single level radiculopathy. Usually seen in the cervicle vertebraļæ¼ļæ¼. Unilateral.
. Usually following forced flexion of the neck

343
Q

What is shy ā€“ Drager syndrome

A

Itā€™s a type of multisystem atrophy. Characterised by parkinsonism, Nigel autonomic dysfunction, and potentially other neurological signs like cerebella operatable issues. Usual anti-Parkinson drugs are ineffective and we focus on intravascular volume expansionļæ¼

344
Q

What is Riley day syndrome

A

What is a recessive disease in Ashkenazi Jews. Characterised by severe autonomic nervous system problems, including severe orthostasis. Alongside poor muscle tone

345
Q

Epidural spinal abscess. Classic triad of symptoms, how to diagnose, how to treat

A

Fever, focal/severe back pain, neurological findings. To diagnose take blood and aspiration cultures, an MRI of the spine. Treat with gold spectrum antibiotics and emergency surgical decompression

346
Q

What can be used as an alternative to diagnose osteomyelitis, if the patient has contraindication for MRI

A

Tagged leukocyte scam

347
Q

MSK findings of NF1

A

Scoliosis and paeudoarthritis

348
Q

Three types of cerebral palsy

A

Spastic, dyskinetic, ataxic

349
Q

Spastic cerebral palsy symptoms

A

One or more limbs affected, hypotonia, commando crawling (diplegiaļæ¼) or paraplegia. Contractures and a equinovarus ļæ¼.

350
Q

Gait type seen in mytonic dystrophy

A

Waddling

351
Q

Gait type seen in mytonic dystrophy

A

Waddling

352
Q

Papilledema vs glaucomaā€¦.. vision loss

A

Papilledema = large blind spot

Glaucoma = peripheral loss first

353
Q

How to tell between cyanotic BHS and tet of fallot

A

Tet of fallot will have hyperventilation. Whereas BHS has breath holdingā€¦ā€¦ā€¦

354
Q

Dx this

1 year old, falls. Minor. But when lands, stop breathing for a min and becomes limp, LOC and pale

A

Pallid BHS

355
Q

Autonomic dysreflexia

A

Spinal cord full lesion above T6. Anything causing high SNS below lesion (bladder distension from BPH for example) is unaaposed, leading to high SNS neurotransmitter and HTN. The brain will oppose this with PNS, causing flush and low hr

356
Q

Meds to avoid in MG

A

Magnesium sulfate
ā€¢ Fluoroquinolones, aminoglycosides
ā€¢ Neuromuscular blocking agents
ā€¢ CNS depressants
ā€¢ Muscle relaxants
ā€¢ Calcium channel blockers
Beta blockers
ā€¢ Opioids
Statins

357
Q

10 Hz pattern on EEG seen in high seizure

A

Tonic clonic

358
Q

Recall our paroxysmal sympathetic nervous system hyperactivity case

A

After traumatic brain injury the brains centres for SNS can get mixed up. So we get times of increased sympathetic system during times of external stimuli

359
Q

Dizziness when patient has lots of work out with arms.

Rui heard left clavicle

A

Subclavian steal syndrome

360
Q

What is trihexyphenidyl

A

An anticholinergic. Fairly good for Parkinsonā€™s

361
Q

Breath holding spell, usually okay, just need to check one thing

A

For iron deficiency

362
Q

Point: never forget you remix an catholyte us, looks very similar to hepatic

A
363
Q

Which is the curtain across blindness

A

More retinal detachment, but not 100% sure

364
Q

Case with history of tripping/falling. Constipation. Microcytic anaemia

A

Lead poisoning

365
Q

Cerebella haemorrhage management

A

Usually surgery, especially if thereā€™s neurological issues, more than 3 cm, brainstem compression, hydro Kefalos.

366
Q

Five components to the NEXUS To tell us one to do spine cervical imagingļæ¼

A

Neuro complication, intoxication, obvious injury, tender spine, AMS

USMLE Step 2 - Top 5% (34 decks)

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