Neuro

Question 2

Symptoms of bulbar palsy

Answer 2

Flaccid, fasciculating tongue, absent/normal jaw jerk, quiet, hoarse or nasal speech, dysphagia and associated drooling

Question 3

Bulbar palsy is due to…

Answer 3

Degeneration of CN IX, x, xi and Xii of LMN type, nerves with nuclei in the medulla

Question 4

DD of bulbar palsy

Answer 4

MND, myasthenia gravis, guillakm-barre, syringobulbia (fluid filled cavities in the brain stem, congenital, trauma or tumour), polio, tumour of brainstem (glioma) Lyme disease, genetic (kennedys syndrome), infarction

Question 5

Findings in pseudo bulbar palsy compared to bp

Answer 5

Exaggerated jaw jerk shows CN V, stiff spastic tongue not wasted, Donald Duck speech, preserved palatal muscles preserved, mood disturbances (eg giggling)

Question 6

Pseudo bulbar palsy is due to damage of…

Answer 6

Cortical bulbar tract bilateral damage must occur for symptoms

Question 7

Causes of pseudo bulbar palsy

Answer 7

Stroke, mnd, ms, severe head injur

Question 8

a cortical lesion of the …… may cause intellectual impairment, personality change, urinary incontinence, monoparesis/hemiparesis. Damage to the …..may also cause brocca’s aphasia

Answer 8

a cortical lesion of the frontal lobe may cause intellectual impairment, personality change, urinary incontinence, monoparesis/hemiparesis. Damage to the left frontal lobe may also cause brocca’s aphasia

Question 9

a cortical lesion of the frontal lobe may cause ……..Damage to the left frontal lobe may also cause …..

Answer 9

a cortical lesion of the frontal lobe may cause intellectual impairment, personality change, urinary incontinence, monoparesis/hemiparesis. Damage to the left frontal lobe may also cause brocca’s aphasia

Question 10

Damage to the…… may cause acalculia (inability to do maths problems), alexia (can’t read), agraphia (can’t write), wernike’s aphasia, R-L disorientation, homonymous field defect.

Answer 10

Damage to the L temporo-parietal lobe may cause acalculia (inability to do maths problems), alexia (can’t read), agraphia (can’t write), wernike’s aphasia, R-L disorientation, homonymous field defect.

Question 11

Damage to the L temporo-parietal lobe may cause ….

Answer 11

Damage to the L temporo-parietal lobe may cause acalculia (inability to do maths problems), alexia (can’t read), agraphia (can’t write), wernike’s aphasia, R-L disorientation, homonymous field defect.

Question 12

Damage to the …. may cause confused states, failure to recognise faces, homonymous field defect

Answer 12

Damage to the R temporal lobe may cause confused states, failure to recognise faces, homonymous field defect

Question 13

Damage to the R temporal lobe may cause ….

Answer 13

Damage to the R temporal lobe may cause confused states, failure to recognise faces, homonymous field defect

Question 14

Damage to ….. may cause contralateral sensory loss/neglect, agraphaesthesia, homonymous field defect

Answer 14

Damage to either parietal lobe may cause contralateral sensory loss/neglect, agraphaesthesia, homonymous field defect

Question 15

Damage to either parietal lobe may cause …..

Answer 15

Damage to either parietal lobe may cause contralateral sensory loss/neglect, agraphaesthesia, homonymous field defect

Question 16

Damage to the …. may specifically cause dressing apraxia and failure to recognise faces

Answer 16

Damage to the right parietal lobe may specifically cause dressing apraxia and failure to recognise faces

Question 17

Damage to the right parietal lobe may specifically cause ….

Answer 17

Damage to the right parietal lobe may specifically cause dressing apraxia and failure to recognise faces

Question 18

Damage to the L parietal lobe may specifically cause ….

Answer 18

limb apraxia

Question 19

Damage to the occipital/occipitoparietal lobe may cause ….

Answer 19

visual field defects, visuospacial defects, disturbances of visual recognition

Question 20

Damage to the ….. may cause visual field defects, visuospacial defects, disturbances of visual recognition

Answer 20

visual field defects, visuospacial defects, disturbances of visual recognition

Question 21

…….may cause partial seizures, focal motor seizures of contralateral limbs, conjugate deviation of head and eyes away from lesion

Answer 21

Irritative cortical lesions to the frontal lobe may cause partial seizures, focal motor seizures of contralateral limbs, conjugate deviation of head and eyes away from lesion

Question 22

Irritative cortical lesions to the frontal lobe may cause ….

Answer 22

Irritative cortical lesions to the frontal lobe may cause partial seizures, focal motor seizures of contralateral limbs, conjugate deviation of head and eyes away from lesion

Question 23

….. may cause formed visual hallucinations, complex paratial seizures, memory disturbances eg deja vu

Answer 23

Irritative cortical lesions to the temporal lobe may cause formed visual hallucinations, complex paratial seizures, memory disturbances eg deja vu

Question 24

Irritative cortical lesions to the temporal lobe may cause …..

Answer 24

Irritative cortical lesions to the temporal lobe may cause formed visual hallucinations, complex paratial seizures, memory disturbances eg deja vu

Question 25

Parietal irritative cortical lesions may cause ……

Answer 25

Parietal seizures may cause focal sensory seizures of contralateral limbs

Question 26

.....may cause focal sensory seizures of contralateral limbs

Answer 26

Parietal irritative cortical lesions

Question 27

Parieto-occipital irritative lesions may cause

Answer 27

crude visual hallucinations (eg, shapes in one part of visual field)

Question 28

..... may cause crude visual hallucinations (eg, shapes in one part of visual field)

Answer 28

Parieto-occipital irritative lesions

Question 29

Occipital irritative lesions may cause

Answer 29

visual disturbances (eg flashes)

Question 30

may cause visual disturbances (eg flashes)

Answer 30

Occipital irritative lesion

Question 31

the lateral lobes of the cerebellum control....

Answer 31

co-ordination of movement of ipsilateral limbs

Question 32

..... maintain axial/midline posture and balance

Answer 32

the vermis/midline structure of the cerebellum maintain axial/midline posture and balance

Question 33

the vermis/midline structure of the cerebellum maintain axial/midline .....posture and balance

Answer 33

axial/midline posture and balance

Question 34

what symptoms will occur with a cerebellum lesion?

Answer 34

DASHING Dysdidokokinesiahw Ataxia (truncal. Broad ataxic gate) Slurred speech Hypotonia and hyporeflexia of limbs Intention tremor with past pointing and dysmetria (movements inprecise in direction/force and distance) and titubation (rhythmic head movement in yes-yes/no-no movements) Nystagmus, course, horizontal with fast component towards lesion

Question 35

what symptoms would occur from a midline/vermis cerebellar lesion?

Answer 35

difficulty standing/sitting unsuppoorted, truncal ataxia (broad ataxic gate), vertigo and vomiting if extending to 4th ventricle

Question 36

vomitting in ataxia will occur if lesion extends to...

Answer 36

4th ventricle

Question 37

nystagmus in cerebellar lesions will be

Answer 37

course, horizontal and have fast component towards lesion

Question 38

what is titubation which occurs due to cerebellar lesions

Answer 38

rhythmic head movements in YES/NO directions

Question 39

what is dysmetria which occurs due to cerebellar lesions

Answer 39

movements inprecise in direction/force and distance

Question 40

what clinical syndromes may arise from a basal ganglia pathology

Answer 40

parkinsonism, huntington's and hemiballismus

Question 41

In a disorder of the basal ganglia there may be....

Answer 41

BAR CHATD Bradykinesia (slowness of speech/movement Akinesia (no movement) Rigidity of muscles Involuntary movements including.... Chorea (jerky involuntary movements) Hemiballismus (violent involuntary movement usually restricted to one arm involving proximal muscles) Athetosis (Writhing involuntary movements usually of hands, face and tongue) Tremor Dystonia (spasms/abnormal muscle control)

Question 42

Describe Hemiballismus

Answer 42

due to basal ganglia lesion. Hemiballismus (violent involuntary movement usually restricted to one arm involving proximal muscles)

Question 43

parkinson's disease is due to

Answer 43

degeneration of the substantia nigra dopaminergic neurones. Pathological hallmark of this is Lewy bodies in this area

Question 44

Signs of Parkinsons

Answer 44

TRAMP Tremor, pill rolling, 4-6 hz Rigidity (lead pipe resistance to passive movement) Akinesia/bradykinesia Monotone voice and expressionless face Postural instability and short, shuffling gate

Question 45

Damage to the ......would cause a bitemporal hemianopia (loss of both temporal visual fields)

Answer 45

Damage to the optic chiasm would cause a bitemporal hemianopia (loss of both temporal visual fields)

Question 46

Damage to the optic chiasm would cause a ......

Answer 46

Damage to the optic chiasm would cause a bitemporal hemianopia (loss of both temporal visual fields)

Question 47

Damage to the optic radiation (parietal/occipital lobe) will cause ......

Answer 47

Damage to the optic radiation (parietal/occipital lobe) will cause contralateral homonymous hemianopia (loss of opposing side of both eye's visual field or loss of nasal visual field in ipsilateral eye and temporal VF in contralateral eye)

Question 48

Damage to the ...... will cause contralateral homonymous hemianopia (loss of opposing side of both eye's visual field or loss of nasal visual field in ipsilateral eye and temporal VF in contralateral eye)

Answer 48

Damage to the optic radiation (parietal/occipital lobe) will cause contralateral homonymous hemianopia (loss of opposing side of both eye's visual field or loss of nasal visual field in ipsilateral eye and temporal VF in contralateral eye)

Question 49

damage to the .... would cause contralateral superior quadrantanopia (damage to upper half of contralateral temporal VF and ipsilateral nasal VF)

Answer 49

damage to the temporal loop of the optic radiation would cause contralateral superior quadrantanopia (damage to upper half of contralateral temporal VF and ipsilateral nasal VF)

Question 50

damage to the temporal loop of the optic radiation would cause ....

Answer 50

damage to the temporal loop of the optic radiation would cause contralateral superior quadrantanopia (damage to upper half of contralateral temporal VF and ipsilateral nasal VF)

Question 51

UMN lesion signs

Answer 51

spastic increase in tone/paralysis, exaggerated tendon reflexes, extensor plantar response, no muscle wasting, loss of fine finger/toe movements, loss of abdominal reflexes, drift of upper limb, normal electrical excitability of muscles

Question 52

LMN lesion signs

Answer 52

weakness/paralysis, wasting, hypotonia, reflex loss, fasciculations contractures of muscle and trophic changes in skin and nails long term

Question 53

definition of TIA

Answer 53

Sudden focal loss, (weak limb, aphasia, loss of vision) lasting less than 24 hours with complete recovery

Question 54

Amaurossi fugax definition

Answer 54

sudden loss of vision in one eye, often occuring with TIA, often 1st clinical evidence of internal carotid stenosis. Also occurs as benign event in migraine

Question 55

definition of stroke

Answer 55

sudden focal deficit lasting more than 24 hours/causing death which has no other apparent cause but vascular

Question 56

what risk factors predispose to a cerbral infarction? by how much?

Answer 56

largely, obesity, diabetes, hypertension, smoking, carotid artery stenosis, moderately inactive lifestyle, alcohol, hypercholesterolaemia, raised haematocrit, AF, sleep apnoea

Question 57

which risk factors predispose someone to a cerbral haemorrhage

Answer 57

largely, hypertension, obesity, smoking and poosibly AF

Question 58

Which factors predispose someone to a stroke from a SAH

Answer 58

smoking and hypertension

Question 59

Describe a SDH

Answer 59

Collection of blood in subdural space following rupture of a vein. Usually follows head injury which can be trivial but can occur spontaneously

Question 60

Which factors predispose somebody to a chronic SDH? why?

Answer 60

Elderly (veins become brittle and taut by shrinkage), alcoholism, reduced blood clotting

Question 61

clinical presentation of chronic SDH

Answer 61

fluctuant symptoms occuring within days/weeks/months, headache, drowsiness, confusion, focal deficits (hemiparesis/sensory loss), personality change, epilepsy (occasionally), stupor, coma and coning could follow

Question 62

how would a CT look in a SDH?

Answer 62

clot plus midline shift, crescent shaped collection of blood over 1 hemisphere which differentiates subdural from extradural

Question 63

differential dx of SDH could also include

Answer 63

cerebral tumour, dementia, evolving stroke

Question 64

abnormalities which commonly predispose to SAH

Answer 64

Berry Aneurysm, 70%, arteriovenous malformation, 20% no lesion found in 10%

Question 65

less common factors predisposing to SAH

Answer 65

Bleeding disorders, endocarditis, acute bacterial meningitis, brain tumours, arteritis (eg SLE), coarctation of aorta, marfan's, ehler's danlos, polycystic kidneys, spinal Arteriovenous malformation

Question 66

signs/symptoms of SAH

Answer 66

* a sudden and severe headache – it has been described as a ‘thunderclap headache’, similar to a sudden hit on the head, resulting in a blinding pain unlike anything ever experienced before, often radiating to back of head * stiff neck * feeling and being sick * loss of consciousness or convulsions (uncontrollable shaking) * stroke-like symptoms such as slurred speech and weakness on one side of the body

Question 67

what is the investigation of choice for a SAH. What will the findings be?

Answer 67

CT. will show blood within48 hrs, can estimate load of blood and grade of lesion, CT angiogram can also be done to show anatomy

Question 68

What test may be performed in suspected SAH if not confirmed by CT? What will be the findings?

Answer 68

Lumbar puncture, will be yellow

Question 69

what can be the complications of SAH

Answer 69

vascular spasm causing widespread ischaemia and swelling around the brain, blockage of CSF drainage causing hydrocephalus. 30% of patients will die immediately, of survivors 30% will rebleed within a year without intervention

Question 70

which organisms account for around 70% of bacterial meningitis cases in adults

Answer 70

Neisseria meningitides and Strep pneumoniae

Question 71

What are the symptoms of autonomic dysfunction

Answer 71

dizziness and fainting upon standing up (orthostatic hypotension) inability to alter heart rate with exercise (exercise intolerance) sweating abnormalities, which could alternately be too much sweat or insufficient sweat digestion difficulties due to slow digestion. Resulting symptoms could include loss of appetite, bloating, diarrhea or constipation, and difficulty swallowing. urinary problems. These can include difficulty starting urination, incontinence, and incomplete emptying of the bladder sexual problems. In men, this could be difficulty with ejaculation and/or maintaining an erection. In women, this could be vaginal dryness and/or difficulty with orgasm vision problems. This could be blurry vision, or the failure of the pupils to react quickly enough to changes in light. Orthostatic hypotension or orthostatic intolerance (a milder form of orthostatic hypotension) are two of the most common conditions resulting from ANS disorders. Orthostatic intolerance, which results in low blood pressure on standing, causes alarming symptoms. These include lightheadedness, fainting, and heart palpitations.

Question 72

what are the typical signs of meningitis?

Answer 72

photophobia, vomiting, malaise, fever, rigors, development in minutes to hours, irritable and prefers to lie still, neck stiffnes, positive kernig's sign, papillodema may develop, meningococcal rash

Question 73

how should a suspected TIA be managed

Answer 73

aspirin (300 mg daily) started immediately specialist assessment[6] and investigation within 24 hours of onset of symptoms measures for secondary prevention introduced as soon as the diagnosis is confirmed, including discussion of individual risk factors

Question 74

When should patients suffering an acute stroke have a brain scan?

Answer 74

1 Brain imaging should be performed immediately[16] for people with acute stroke if any of the following apply: indications for thrombolysis or early anticoagulation treatment on anticoagulant treatment a known bleeding tendency a depressed level of consciousness (Glasgow Coma Score below 13) unexplained progressive or fluctuating symptoms papilloedema, neck stiffness or fever severe headache at onset of stroke symptoms. 1.3.2.2 For all people with acute stroke without indications for immediate brain imaging, scanning should be performed as soon as possible[17] .

Question 75

Investigations for patient with suspected stroke

Answer 75

``` Serum glucose levels Complete blood count (CBC) Electrolyte values Prothrombin time (PT) Activated partial thromboplastin time (aPTT) ```

Question 76

Which screening tools can be used to assess the likelihood of a patient having a stroke?

Answer 76

Community, FAST (Face, Arms, Speech, Time) Hospital, more complicated such as ROSIER scoring (-ve marks for recent seizures/LOC/Syncope, +ve for face, arms, legs, speech, visual field)

Question 77

How is muscle power graded in neuro exam

Answer 77

``` 0 nil 1 flicker of movement 2 movement cannot overcome gravity 3 movement cannot overcome any resistance 4 movement is weaker than normal 5 normal ```

Question 78

What pattern of weakness is usually seen in an UMN lesion

Answer 78

flexors > extensors in upper limbs | extensors > flexors in lower limbs

Question 79

Upper motor neurone lesions occur when the damage is above....

Answer 79

the anterior horn

Question 80

When should lumbar puncture not be performed

Answer 80

GCS <9m suspect raised ICP, bradycardia/hypertension, focal neuro signs, unequal poorly responsive pupils, papilodema, shock, convulsions, coagulation abnormalities, respiratory insufficiency

Question 81

What signs can be observed for in parkinsons

Answer 81

Inspection Look for: - Hypomimia (decreased facial expression) - Blepharoclonus (fine eyelid tremor) - Resting tremor (brought out by distraction - such as conversation) - Tardive dyskinesia (chewing movements of the mouth - drug treatment side effect) [Return to top] Face Look for: - glabellar tap (keep blinking - normally adjust) - normal eye movements but abnormal vertical gaze + VOR (in supranuclear palsy) - speech ? monotonous voice

Question 82

What additional examinations can be done in a patient with parkinsons

Answer 82

Thank the patient and offer to assist them to get dressed again Offer to do mmse for Lewis body Offer to take lying and standing blood pressure (autonomic function may be affected in 'Multi-System Atrophy' - MSA) Offer to assess the cerebellar system (this can also be impaired in MSA) Offer to examine the drugs chart (metoclopramide and neuroleptics can cause Parkinsonian symptoms) Offer to examine their visual tracking for signs of Progressive Supranuclear Palsy (PSP). Ask the patient to hold their head still and follow your finger with their eyes whilst you move it up in a vertical plane in front of their face. Then, test for the 'vestibulo-ocular reflex' by asking the patient to fix their eyes on a point on the far wall, and then move their head up and down by flexing their neck. If a patient is unable to track your finger movements in a vertical plane, but has a retained vestibulo-ocular reflex, then this suggests that there is a supranuclear lesion - in keeping with PSP when it exists with other Parkinsonism signs.

Question 83

What are the parkinsons plus conditions

Answer 83

Progressive super nuclear palsy, multiple system atrophy (autonomic dysfunction eg postural hypo. Disturbances in urination and sexual function) Cortico basal degen. These will lead to cerebellar and cranial nerve funcs eg swallowing, Lewis body dementia

Question 84

What is the differential diagnosis of parkinsons

Answer 84

Parkinsons plus; progressive supranuclear palsy, cortico basal degeneration, multiple system atrophy, Lewis body, drug induced (dopamine agonists eg antipsychotics rispiradone), vascular eg stroke basal ganglia or vascular dementia

Question 85

What are the causes of optic neuritis

Answer 85

The most common cause of ON in regions where MS is relatively common (Caucasian populations and high latitudes). Ischaemic optic neuropathies Giant cell arteritis (cranial arteritis), anterior and posterior optic neuropathy, diabetic papillopathy. Corticosteroid-responsive ON Autoimmune diseases, including sarcoidosis, systemic lupus erythematosus,[5] Behçet's disease, neuromyelitis optica (Devic's syndrome - affects optic nerves and the spinal cord),[6][7] autoimmune ON, chronic relapsing inflammatory ON. Other inflammatory causes Post-infection, post-vaccination, neuroretinitis, acute disseminated encephalomyelitis.