Neurology & Neurosurgery

Question 1

brain lesion on the left side

Answer 1

body symptoms on right side

Question 2

List of anticholinergics

Answer 2

• Banzhexol
• Levodopa

Question 3

Brain tumour vs brain abscess

Answer 3

brain tumour enhance on contrast CT

Question 4

-Rapidly fluctuating cognition + Visual hallucinations + Spontaneous motor Parkinsonism

Answer 4

Lewy bodies

Question 5

Cardinal symptom of dementia with Lewy bodies

Answer 5

Visual hallucinations

Question 6

Ptosis + Myosis + anhidrosis

Answer 6

Horner’s syndrome

Question 7

ptosis + mydriasis

Answer 7

3rd CN palsy

Ptosis (drooping of the upper eyelid) combined with mydriasis (dilated pupil) is a clinical presentation that often points to specific underlying neurological conditions. Here are the primary considerations and diagnostic steps for such a presentation:

Question 8

Most common cause 3rd CN palsy

Answer 8

Diabetic neuropathy

Question 9

key feature of DM 3rd nerve palsy

Answer 9

Normal pupillary reflex

Question 10

common cause of 6th nerve palsy

Answer 10

diabetes

Question 11

6th nerve palsy diseases

Answer 11

• diabetes
• Meningitis
• multiple sclerosis
• Wernicke’s encephalopathy
• nasopharyngeal tumour

Question 12

Ramsay Hunt syndrome treatment

Answer 12

valacyclovir/acyclovir 7 to 10 days + prednisone 5 days

Question 13

Campylobacter jejuni + Normal cell count + high protein with some neurological defects

Answer 13

Guillain-Barre syndrome

Question 14

muscular weakness +
mild distal sensory loss

Answer 14

Guillain-Barre syndrome

Question 15

Guillain-Barre syndrome respiratory investigation

Answer 15

Forced vital capacity

Question 16

Guillain-Barre syndrome treatment

Answer 16

• IV immune globulin
• plasma exchange,
  -for severe cases, mechanical ventilation

Question 17

most common parotid tumour

Answer 17

pleomorphic adenoma

Question 18

slow growing + parotid gland

Answer 18

pleomorphic adenoma

Question 19

fast growing + parotid gland involvement + causing symptoms

Answer 19

pleomorphic carcinoma

Question 20

Unilateral headaches
+ nasal stuffiness + conjunctival injection + lacrimation

Answer 20

Cluster headache

Question 21

Cluster headache acute treatment

Answer 21

100% oxygen

Question 22

Cluster headache prophylaxis

Answer 22

CCB

Question 23

Unilateral headaches +

Question 24

SS vs NMS

Answer 24

SS: hyperreflexia + nausea/vomiting
NMS: hyporeflexia

Question 25

short hx of unilateral facial droop + dysphasia

Answer 25

CAS/TIA

Question 26

TIA dx
Investigations

Answer 26

Initial: Carotid artery doppler US
Best: CTPA

Question 27

Parkinsons disease

Answer 27

U/L tremors
Good response to Levodopa

Question 28

CAS referral cut-off

Answer 28

Asymptomatic:
- < 80% + yearly follow-up with CDUS
- >80 + refer

Symptomatic:
- <50% medical therapy + antiplatelet + follow-up
- >50% surgery -2 weeks of event + medical therapy

Question 30

pain in lateral shin + dorsum of foot + weakness of eversion + dorsiflexion

Answer 30

Common peroneal nerve injury

Pain in the lateral shin and dorsum of the foot with associated weakness in eversion and dorsiflexion is indicative of common peroneal nerve involvement.

Question 31

diabetic neuropathy treatment

Answer 31

TCA

Tricyclic Antidepressants (TCAs) for Diabetic Neuropathy:

Common TCAs Used:

1.	Amitriptyline
2.	Nortriptyline
3.	Imipramine
4.	Desipramine

Question 32

peripheral neuropathy investigation

Answer 32

1. Check B12 level as this can be low -metformin can lead to low b12.
   2.thyroid function tests to assess for hypothyroidism.
2. Assess for autoimmune neuropathy

Question 33

family hx + acute painful eye loss of vision + hyperreflexia + increase tone

Answer 33

multiple sclerosis (MS)

Question 34

Migraine treatment

Answer 34

• BB (propranolol)
• TCA
• pizotifen,
• sodium valproate

RACGP

Nonmigraine specific analgesics
Aspirin (900 mg)
Paracetamol (1000 mg or as required)
Naproxen (500-1000 mg or as required)
Ibuprofen ( 400-800 mg)
Oral antiemetics
Metoclopramide (Maxolon) (10 mg)
Prochlorperazine (Stemetil) (5-10 mg)
Domperidone (Motilium) (10 mg)
Migraine specific medications
Ergotamine preparations
Ergotamine with caffeine
Triptan preparations

Question 35

Migraine treatment in children

Answer 35

1st line: Ibuprofen
2nd: paracetamol

Question 36

severe “thunderclap” a headache + loss of consciousness

Answer 36

SAH

Question 37

most common cause of SAH

Answer 37

Rupture of saccular aneurysm

Question 38

most common location of SAH

Answer 38

anterior circulation on the circle of Willis 85%

Question 39

Post SAH + stiffness + photophobia + hyperreflexia + unilateral weakness

treatment
What do you give?

Answer 39

Nimodipine
-decreases the probability of stroke

Question 40

SAH complications

Answer 40

• Re-rupture
• Hyponatremia
• Hydrocephalus
• Hydrocephalus

Question 41

clock drawing test assesses

Answer 41

severity of dementia

Question 42

clock drawing test

Answer 42

Frontal and Temporo-parietal functioning

The frontal lobe is like the brain’s control panel, responsible for many important skills and behaviors. Here are its main functions in simple terms:

1. Planning and Decision-Making:
   
   • Helps you make decisions, plan for the future, and solve problems.
2. Movement Control:
   
   • Directs voluntary movements through the motor cortex.
3. Speech Production:
   
   • Broca’s area, located in the frontal lobe, is crucial for producing speech.
4. Behavior and Emotional Control:
   
   • Involves managing your emotions, behavior, and impulses.
5. Personality:
   
   • Influences your personality traits and social behavior.

The temporo-parietal junction (TPJ) is where the temporal and parietal lobes meet. It’s involved in various complex processes. Here are its main functions in simple terms:

1. Attention and Awareness:
   
   • Helps you focus on specific tasks and become aware of your surroundings.
2. Language and Understanding:
   
   • Involves comprehension of spoken and written language.
3. Social Cognition:
   
   • Important for understanding other people’s thoughts, intentions, and emotions.
4. Sensory Integration:
   
   • Integrates sensory information from different parts of the brain, helping you understand spatial relationships and navigate the world.

By working together, the frontal lobe and temporo-parietal junction enable you to plan, move, speak, control emotions, focus, understand language, and interact socially.

Question 43

occupational therapist / ophthalmologist referral to drive

Answer 43

persistent hemianopia after stroke

Question 44

Permanent commercial driving restriction

Answer 44

1. stable angina
2. ICD (defibrillator)

Question 45

diseases that cause neck stiffness

Answer 45

– Meningitis.
– Subarachnoid haemorrhage.
– Tetanus.
– Upper lobe pneumonia.
– Tender posterior cervical adenopathy.
– Retropharyngeal abscess.
– Rheumatoid arthritis

Question 46

degenerative disease of the central nervous system caused by infectious proteins

Answer 46

Creutzfeldt-Jakob disease (CJD)
prion

Question 47

restless leg syndrome dx

Answer 47

clincal + Iron studies

Question 48

restless leg syndrome treatment

Answer 48

Dopamine agonist:
- ropinirole
- levodopa

Question 49

Alzheimer’s vs Fronto-temporal dementia

Answer 49

• behavioural change early in fronto-temporal

Question 50

Alzheimer EEG

Answer 50

Generalized background slowing

Electroencephalography (EEG) can provide supportive diagnostic information in Alzheimer’s disease (AD), although it is not typically used as a primary diagnostic tool for this condition. In Alzheimer’s disease, the EEG findings often show generalized background slowing.

Generalized Background Slowing on EEG in Alzheimer’s Disease:

1.	Generalized Slowing:
•	In the early stages of Alzheimer’s disease, EEG may show a diffuse slowing of the background rhythm.
•	This is characterized by a reduction in the frequency of the normal alpha rhythm (8-13 Hz) and an increase in theta (4-7 Hz) and delta (0.5-3 Hz) waves.
2.	Decreased Alpha Activity:
•	There is a reduction in the posterior dominant rhythm, which normally consists of alpha waves.
•	This decrease in alpha activity is indicative of generalized cerebral dysfunction.
3.	Increased Theta and Delta Activity:
•	The presence of increased slow waves (theta and delta) across the EEG is typical.
•	These slow waves indicate a slowing of neuronal activity and are reflective of the brain’s impaired function due to the neurodegenerative processes in Alzheimer’s disease.

Clinical Implications:

•	Correlation with Disease Severity: The degree of EEG slowing often correlates with the severity of cognitive impairment. More pronounced slowing is generally associated with more advanced stages of Alzheimer’s disease.
•	Differentiation from Other Dementias: While generalized slowing is common in Alzheimer’s disease, it can also be seen in other types of dementia. EEG findings need to be interpreted in conjunction with clinical assessment, neuroimaging, and other diagnostic tests.

Conclusion:

Generalized background slowing on EEG is a common finding in Alzheimer’s disease, reflecting widespread neuronal dysfunction. Although not a primary diagnostic tool, EEG can provide additional information, particularly in differentiating Alzheimer’s from other neurological conditions and assessing the progression of cognitive impairment.

Question 51

Alzheimer’s lobe atrophy

Answer 51

frontotemporal lobe atrophy

Question 52

medications avoided in patients with rest less leg syndrome

Answer 52

– Metoclopramide (dopamine antagonists)
– Droperidol (dopamine antagonists)
– Lithium
– Naloxone (opioid antagonist)
– Antidepressants that increase serotonin levels

In patients with Restless Legs Syndrome (RLS), certain medications should be avoided because they can exacerbate the symptoms. The medications listed below are known to potentially worsen RLS:

• Metoclopramide: Often used for nausea and gastrointestinal issues, but it can block dopamine receptors and worsen RLS symptoms.
• Droperidol: Used for nausea and as a sedative, also blocks dopamine receptors and can exacerbate RLS.

• Lithium: Commonly used for bipolar disorder, but can worsen RLS symptoms due to its impact on dopamine regulation.

• Naloxone: Used to reverse opioid overdoses, but by blocking opioid receptors, it can worsen RLS symptoms, as some opioid medications are actually used to treat severe cases of RLS.

• Selective Serotonin Reuptake Inhibitors (SSRIs) and Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs):
  
  • Medications like fluoxetine (Prozac), sertraline (Zoloft), and venlafaxine (Effexor) can worsen RLS symptoms. These medications increase serotonin levels, which can impact dopamine pathways and exacerbate RLS.

• Antipsychotics: Medications like haloperidol (Haldol) and risperidone (Risperdal) can also worsen RLS due to their dopamine-blocking effects.
• Antihistamines: Particularly the older, sedating types like diphenhydramine (Benadryl), which can worsen RLS symptoms.

When managing a patient with RLS, it’s crucial to review their medication list and avoid those that can exacerbate symptoms. For necessary medications that might worsen RLS, consider alternatives or consult with a specialist for appropriate management strategies. In cases where these medications are essential and cannot be discontinued, adjusting the treatment for RLS or adding medications specifically to manage RLS symptoms may be necessary. Always tailor the approach to the individual patient’s needs and response to treatment.

Question 53

unexplained falls + axial rigidity + dysphagia +
vertical gaze deficits

Answer 53

supranuclear palsy

The symptoms of unexplained falls, axial rigidity, dysphagia, and vertical gaze deficits are characteristic of Progressive Supranuclear Palsy (PSP).

Progressive Supranuclear Palsy is a neurodegenerative disorder characterized by the following core features:

1. Unexplained Falls:
   
   • Patients with PSP often experience frequent and unexplained falls, typically backward (retropulsion).
2. Axial Rigidity:
   
   • Stiffness and rigidity primarily affecting the neck and trunk, as opposed to the limbs. This axial rigidity contributes to postural instability and difficulty with movement.
3. Dysphagia:
   
   • Difficulty swallowing is a common symptom and can lead to aspiration and nutritional issues.
4. Vertical Gaze Palsy:
   
   • Difficulty in voluntary vertical eye movements, particularly downward gaze. This supranuclear ophthalmoplegia is a hallmark of PSP and can lead to significant difficulties with vision and balance.

• Bradykinesia: Slowness of movement.
• Dysarthria: Difficulty speaking due to motor control problems of the speech muscles.
• Cognitive Impairment: Executive dysfunction, such as difficulties with planning, organizing, and multitasking.

• Clinical Evaluation: Diagnosis is primarily clinical, based on history and physical examination. The combination of the above symptoms strongly suggests PSP.
• Imaging: MRI may show characteristic changes, such as midbrain atrophy (hummingbird sign or penguin sign) and may help rule out other causes.
• Response to Treatment: Unlike Parkinson’s disease, PSP typically does not respond well to dopaminergic treatments like levodopa.

• Symptomatic Treatment: Focuses on managing symptoms since there is no cure for PSP.
  
  • Physical Therapy: To address balance and mobility issues.
  • Speech Therapy: For dysarthria and dysphagia.
  • Medications: Limited benefit, but some patients might receive medications like amantadine or levodopa/carbidopa for symptomatic relief.
• Supportive Care:
  
  • Nutritional support and possibly feeding tube placement for severe dysphagia.
  • Safety modifications at home to prevent falls.
  • Occupational therapy for assistance with daily living activities.

Progressive Supranuclear Palsy is characterized by unexplained falls, axial rigidity, dysphagia, and vertical gaze deficits. It is diagnosed based on clinical features, supported by imaging studies. Treatment is primarily supportive and aimed at improving quality of life and managing symptoms.

Question 54

ataxia + falls + past pointing + positive Romberg’s sign
+ nystagmus

Answer 54

Cerebellar stroke

A cerebellar stroke typically presents with several hallmark signs and symptoms that reflect dysfunction in the cerebellum, which is responsible for coordinating movement and balance. The symptoms you’ve listed are characteristic of a cerebellar stroke:

1. Ataxia:
   
   • A lack of voluntary coordination of muscle movements. This can affect the limbs (limb ataxia), trunk (truncal ataxia), and gait (gait ataxia).
2. Falls:
   
   • Due to impaired coordination and balance, patients are prone to falling, often without warning.
3. Past Pointing:
   
   • Inability to accurately target movements, especially noticeable in the finger-to-nose test. The patient may overshoot or undershoot the intended target.
4. Positive Romberg’s Sign:
   
   • Difficulty maintaining balance when standing with feet together and eyes closed. Although typically associated with sensory ataxia, a positive Romberg’s sign can also occur in cerebellar ataxia when visual input is removed, revealing underlying instability.
5. Nystagmus:
   
   • Involuntary, rhythmic eye movements. These can be horizontal, vertical, or rotary and are often a sign of cerebellar involvement.

• Dysarthria: Slurred or scanning speech due to poor coordination of the muscles used in speaking.
• Dysmetria: Inability to control the distance, power, and speed of a movement.
• Dysdiadochokinesia: Difficulty with rapid alternating movements.
• Vertigo: A sensation of spinning or dizziness, often accompanied by nausea and vomiting.

1. Clinical Evaluation:
   
   • A detailed neurological examination assessing coordination, balance, eye movements, and speech can help identify cerebellar dysfunction.
2. Imaging:
   
   • CT Scan: May show areas of infarction or hemorrhage in the cerebellum.
   • MRI: More sensitive and specific for detecting acute ischemic strokes in the cerebellum.
3. Other Tests:
   
   • Blood Tests: To assess for risk factors and underlying causes (e.g., clotting disorders).
   • Echocardiogram: To look for sources of emboli from the heart.
   • Carotid Doppler Ultrasound: To assess for carotid artery disease.

1. Acute Management:
   
   • Stabilization: Ensuring airway, breathing, and circulation are stable.
   • Thrombolysis: If the patient presents within the therapeutic window for thrombolytic therapy (typically within 4.5 hours for ischemic stroke).
   • Antiplatelet Therapy: Aspirin or other antiplatelet agents to prevent further clot formation.
2. Secondary Prevention:
   
   • Anticoagulation: If there is a cardioembolic source.
   • Control of Risk Factors: Management of hypertension, diabetes, hyperlipidemia, and lifestyle modifications (e.g., smoking cessation, diet, exercise).
3. Rehabilitation:
   
   • Physical Therapy: To improve coordination, strength, and balance.
   • Occupational Therapy: To assist with activities of daily living.
   • Speech Therapy: If dysarthria is present.
4. Monitoring and Follow-up:
   
   • Regular follow-up with neurology and primary care to monitor recovery and manage ongoing risk factors.

Cerebellar strokes present with ataxia, falls, past pointing, positive Romberg’s sign, and nystagmus, among other symptoms. Diagnosis is primarily clinical, supported by imaging studies. Acute management focuses on stabilizing the patient and preventing further stroke, while long-term management involves rehabilitation and risk factor modification.

Question 55

resting tremors + cogwheel rigidity +
bradykinesia + festinating gait

Answer 55

Parkinson’s disease

Question 56

Parkinson speech decrement

Answer 56

Progressively inaudible speech

Question 57

Parkinson’s disease vs Drug-induced parkinsonism

Answer 57

drug induced:
- bilateral bradykinesia/tremor
- disappear when the offending agent is ceased
- inadequate response to anti-cholinergic agents

Parkinson’s:
- Asymmetric symptoms
- dramatic response to anti-cholinergics
- Dementia
- presence of tremors

Question 58

Carbidopa/levodopa + dyskinesias + intense akinesia / uncontrollable hyperactivity

Answer 58

Drug-induced dyskinesias

Question 59

Drug-induced dyskinesias treatment

Answer 59

1st: reduction in dopaminergic supplementation
2nd: alternate medication like amantadine, pergolide

Symptoms of Drug-Induced Dyskinesias:

•	Orofacial Movements: Grimacing, tongue protrusion, lip smacking, puckering, and blinking.
•	Limb Movements: Rapid, jerky movements (chorea) or slow, writhing movements (athetosis).
•	Trunk Movements: Twisting or contorting movements.
•	Generalized Restlessness: May feel the need to move constantly (akathisia).

Question 60

High frequency stimulation for Parkison’s aims at which areas

Answer 60

Globus pallidus, subthalamic nucleus, thalamus

Question 61

most significant risk factor for falls in elderly

Answer 61

Visual impairment

Question 62

action tremor which gets worse with doing activity

Answer 62

distal essential tremor

Question 63

essential tremor treatment

Answer 63

1st line: Propranolol and primidone

Question 64

tremor which occurs at rest

Answer 64

Parkinsons

Question 65

resting tremor treatment

Answer 65

anticholinergics
- Benzhexol
- benztropine

Question 66

children / young adults + hepatic
failure +rigidity + clumsy gait + dysarthria + copper

Answer 66

Wilson’s disease

Question 67

Acalculia + Dysgraphia + Finger anomia + -Right-left confusion

Answer 67

Gerstmann’s syndrome

Gerstmann’s syndrome is a neurological disorder characterized by a specific constellation of symptoms, typically resulting from damage to the dominant hemisphere of the brain, particularly the parietal lobe. It was first described by Josef Gerstmann, a German neurologist, in 1924. The syndrome is characterized by a tetrad of symptoms:

1. Agraphia: Difficulty with writing. This includes impaired ability to write words spontaneously or to write according to dictation.
2. Acalculia: Difficulty with performing arithmetic calculations. Patients may have trouble with basic mathematical operations such as addition, subtraction, multiplication, and division.
3. Finger agnosia: Inability to differentiate between fingers or recognize one’s own fingers. This can manifest as difficulty naming or identifying fingers when asked.
4. Left-right confusion: Difficulty distinguishing between left and right directions. Patients may have trouble identifying their own left and right sides or those of others.

• Alexia: Some patients may also exhibit alexia, which is difficulty with reading.

Gerstmann’s syndrome is typically associated with damage to the angular gyrus of the dominant hemisphere, which is located in the parietal lobe. Common causes include:

• Stroke: Particularly involving the left hemisphere.
• Traumatic brain injury: Damage to the parietal lobe from head trauma.
• Brain tumors: Tumors affecting the parietal lobe.
• Degenerative diseases: Such as Alzheimer’s disease or other forms of dementia that affect the parietal lobe.

Diagnosis of Gerstmann’s syndrome involves a thorough neurological examination to assess for the presence of the tetrad of symptoms. Imaging studies, such as MRI or CT scans, may be performed to identify structural abnormalities in the brain, such as tumors or infarcts, that could be causing the symptoms.

Treatment of Gerstmann’s syndrome focuses on addressing underlying causes, if possible, and providing supportive care. This may include:

• Speech and language therapy: To help patients compensate for writing and arithmetic difficulties.
• Occupational therapy: To improve fine motor skills and activities of daily living.
• Cognitive rehabilitation: Strategies to help with memory, attention, and executive function.

The prognosis of Gerstmann’s syndrome depends on the underlying cause and extent of brain damage. Improvement in symptoms can vary widely depending on the individual and the severity of the brain injury.

In summary, Gerstmann’s syndrome is a neurological condition characterized by a specific set of symptoms including agraphia, acalculia, finger agnosia, and left-right confusion. It typically results from damage to the dominant parietal lobe of the brain and can be caused by various conditions affecting this area. Treatment focuses on addressing underlying causes and providing supportive therapies to manage symptoms and improve quality of life.

Question 68

Gerstmann’s syndrome lesion location

Answer 68

Inferior parietal lobule (usually left)

Gerstmann’s syndrome is a neurological disorder characterized by a specific constellation of symptoms, typically resulting from damage to the dominant hemisphere of the brain, particularly the parietal lobe. It was first described by Josef Gerstmann, a German neurologist, in 1924. The syndrome is characterized by a tetrad of symptoms:

1. Agraphia: Difficulty with writing. This includes impaired ability to write words spontaneously or to write according to dictation.
2. Acalculia: Difficulty with performing arithmetic calculations. Patients may have trouble with basic mathematical operations such as addition, subtraction, multiplication, and division.
3. Finger agnosia: Inability to differentiate between fingers or recognize one’s own fingers. This can manifest as difficulty naming or identifying fingers when asked.
4. Left-right confusion: Difficulty distinguishing between left and right directions. Patients may have trouble identifying their own left and right sides or those of others.

• Alexia: Some patients may also exhibit alexia, which is difficulty with reading.

Gerstmann’s syndrome is typically associated with damage to the angular gyrus of the dominant hemisphere, which is located in the parietal lobe. Common causes include:

• Stroke: Particularly involving the left hemisphere.
• Traumatic brain injury: Damage to the parietal lobe from head trauma.
• Brain tumors: Tumors affecting the parietal lobe.
• Degenerative diseases: Such as Alzheimer’s disease or other forms of dementia that affect the parietal lobe.

Diagnosis of Gerstmann’s syndrome involves a thorough neurological examination to assess for the presence of the tetrad of symptoms. Imaging studies, such as MRI or CT scans, may be performed to identify structural abnormalities in the brain, such as tumors or infarcts, that could be causing the symptoms.

Treatment of Gerstmann’s syndrome focuses on addressing underlying causes, if possible, and providing supportive care. This may include:

• Speech and language therapy: To help patients compensate for writing and arithmetic difficulties.
• Occupational therapy: To improve fine motor skills and activities of daily living.
• Cognitive rehabilitation: Strategies to help with memory, attention, and executive function.

The prognosis of Gerstmann’s syndrome depends on the underlying cause and extent of brain damage. Improvement in symptoms can vary widely depending on the individual and the severity of the brain injury.

In summary, Gerstmann’s syndrome is a neurological condition characterized by a specific set of symptoms including agraphia, acalculia, finger agnosia, and left-right confusion. It typically results from damage to the dominant parietal lobe of the brain and can be caused by various conditions affecting this area. Treatment focuses on addressing underlying causes and providing supportive therapies to manage symptoms and improve quality of life.

Question 69

Loss of the ability to recognize items based on touch Loss of the ability to recognize items based on touch

Answer 69

posterior parietal lobe

The ability to recognize items by touch is controlled by a part of the brain called the posterior parietal lobe. This area helps your brain make sense of what you’re feeling with your hands.

• The posterior parietal lobe takes the information from your touch (like shape, texture, and size) and helps you identify what an object is without looking at it.

• If the posterior parietal lobe is damaged, your brain can’t process the touch information correctly.
• As a result, even though you can feel the object, you might not be able to recognize what it is just by touch.

• Think of the posterior parietal lobe as a “touch translator” for your brain. If this translator stops working, you lose the ability to “read” objects with your hands.

Question 70

Gerstmann’s syndrome affects which side

Answer 70

contralateral to upper limbs presentation

Question 71

URTI+ acute onset of vertigo + An absence of tinnitus and hearing loss

Answer 71

Vestibular Neuritis

Question 72

Dix-Hallpike Test +ve

Answer 72

Likely BPPV

Question 73

“raccoon eyes” + blood behind the ears + mastoid ecchymosis (battle)

Answer 73

Basilar skull fracture

Question 74

vascular dementia features

Answer 74

-Sudden onset of memory decline after a stroke with step-wise deterioration
-Variable cognitive impairment and emotional lability.
-Gait abnormalities.
-Urinary dysfunction.
-Parkinsonian motor features.
-Vascular lesions on MRI/CT.

Question 75

vascular dementia treatment

Answer 75

• prevent strokes
• control hypertension

Question 76

vascular dementia memory treatment

Answer 76

acetylcholinesterase inhibitor (donepezil)

Question 77

dementia protective factor
Diet

Answer 77

diet rich in polyunsaturated and monounsaturated fats
(nuts, salmon)

Question 78

raised ICP causes

Answer 78

●Parenchymal brain swelling
●Interstitial and vasogenic Edema
●Alterations in cerebral blood volume (CBV)
●Obstruction of CSF outflow
●Focal cerebral perfusion deficits
●Variable levels of CBF
●Cerebrovascular carbon dioxide (CO) reactivity
●Cerebral vasculitis

Question 79

Posterior column syndrome

Answer 79

bilateral loss of proprioception below the lesion,
preservation of pain and
temperature sensation

Posterior column syndrome, also known as posterior column dysfunction or posterior cord syndrome, is a neurological condition characterized by dysfunction or damage to the posterior columns of the spinal cord. These columns are responsible for transmitting sensory information related to vibration, proprioception (sense of body position), and fine touch to the brain.

Posterior column syndrome can be caused by various conditions that affect the spinal cord, including:

1. Spinal Cord Injury: Trauma to the spine, such as from a motor vehicle accident or a fall, can damage the posterior columns.
2. Tumors: Intramedullary spinal cord tumors or extramedullary tumors compressing the spinal cord can lead to posterior column dysfunction.
3. Degenerative Diseases: Conditions like multiple sclerosis or subacute combined degeneration (often due to vitamin B12 deficiency) can affect the spinal cord’s posterior columns.
4. Vascular Issues: Stroke or spinal cord infarction affecting the posterior circulation can result in this syndrome.

The symptoms of posterior column syndrome typically include:

• Proprioception Deficits: Difficulty in sensing the position and movement of the limbs and body.
• Vibration Sense Impairment: Reduced ability to feel vibrations through a tuning fork or other vibratory stimuli.
• Loss of Fine Touch Sensation: Decreased sensitivity to light touch, such as the ability to detect textures or distinguish between two points touching the skin closely together (two-point discrimination).
• Unsteady Gait: Difficulty walking due to impaired proprioception, which affects balance and coordination.

Diagnosis of posterior column syndrome involves a thorough neurological examination to assess sensory function, including vibration sense, proprioception, and fine touch. Imaging studies such as MRI of the spine may be done to identify structural abnormalities or lesions affecting the posterior columns.

Treatment of posterior column syndrome depends on the underlying cause:

• Trauma: Initial stabilization and surgical intervention may be necessary for spinal cord injuries.
• Tumors: Treatment involves surgical resection, radiation therapy, or chemotherapy depending on the nature of the tumor.
• Degenerative Diseases: Management includes addressing the underlying condition, such as vitamin B12 supplementation in cases of deficiency or disease-modifying therapies in multiple sclerosis.
• Rehabilitation: Physical therapy and occupational therapy play crucial roles in improving mobility, balance, and overall function.

The

Question 80

most common manifestation of muscle weakness with myasthenia gravis

Answer 80

Ocular muscle weakness

Question 81

myasthenia gravis disease location

Answer 81

Neuromuscular junction

Question 82

Myasthenia Gravis best diagnostic test

Answer 82

Single-fibre electromyography

Question 83

pubertal patient + inferior portion iris Lisch nodules + an optic pathway glioma + Ectropion uveae

Answer 83

neurofibromatosis type 1 (NF1)

Question 84

down syndrome most likely to develop what disease

Answer 84

Alzheimer disease

Question 85

diabetic foot ulcers risk factors

Answer 85

• diabetic neuropathy 80%
• previous foot ulceration
• vascular disease,
• foot deformity

Question 86

diabetic foot ulcers assessment

Answer 86

Monofilament testing

Monofilament testing is a simple and effective method used to assess the risk of diabetic foot ulcers. It evaluates the sensory perception in the feet of individuals with diabetes, helping to detect early signs of neuropathy (nerve damage). Here’s how it works:

1. Tool: A monofilament is a thin, flexible, nylon fiber usually calibrated to apply a specific amount of pressure (commonly 10 grams).
2. Procedure:
   
   • The patient should be seated and relaxed, with feet cleaned and dried.
   • The tester uses the monofilament to apply gentle pressure to specific sites on the sole of the foot (commonly the big toe, the base of the toes, and the heel).
   • The filament is pressed against the skin until it bends slightly, ensuring consistent pressure is applied.
   • The patient indicates if they feel the touch.
3. Assessment:
   
   • If the patient cannot feel the monofilament at one or more sites, it suggests a loss of protective sensation, indicating neuropathy and an increased risk for foot ulcers.
   • Areas tested should be marked on a foot diagram for future reference and comparison.

Monofilament testing is an important part of regular diabetic foot assessments to prevent complications and ensure early intervention.

Question 87

recurrent continuous convulsions > 5 mins

Answer 87

status epilepticus

Question 88

status epilepticus treatment

Answer 88

IV diazepam/lorazepam

Question 89

Alzheimer’s medication

Answer 89

Donepezil

Question 90

alcoholic + rapid correction of hyponatremia + quadriplegia

Answer 90

central pontine
myelinolysis (CPM)

Central pontine myelinolysis (CPM) is a serious neurological condition that happens when there’s rapid damage to the protective covering (myelin) of nerve cells in the middle of the brainstem (the pons). This often occurs due to a rapid correction of low sodium levels in the blood. Symptoms can include difficulty speaking and swallowing, weakness, and paralysis.

CPM is primarily caused by rapid changes in serum sodium levels, particularly a rapid increase in sodium levels (hyponatremia corrected too quickly). The exact mechanism is not fully understood, but it is believed to involve osmotic stress and the response of oligodendrocytes (cells that produce myelin) to rapid changes in osmolarity.

• Hyponatremia: Particularly when corrected too rapidly.
• Liver Transplantation: Especially in the context of rapid correction of hyponatremia post-transplant.
• Alcoholism: Chronic alcohol abuse can predispose individuals to electrolyte imbalances.
• Malnutrition: Severe malnutrition or eating disorders that lead to electrolyte disturbances.
• Electrolyte Imbalances: Other electrolyte disturbances, though less common than rapid correction of hyponatremia.

The symptoms of CPM can vary widely depending on the severity and location of the damage. Common clinical features include:

• Quadriplegia: Severe weakness or paralysis affecting all four limbs.
• Dysphagia: Difficulty swallowing.
• Dysarthria: Difficulty speaking.
• Impaired Consciousness: Ranging from confusion to coma in severe cases.
• Cognitive Changes: Such as behavioral changes, confusion, and altered mental status.
• Ocular Abnormalities: Including gaze abnormalities or impaired eye movements.

Diagnosis of CPM is typically based on clinical findings and imaging studies, particularly MRI of the brain. MRI may show characteristic changes in the central pons, including hyperintensity on T2-weighted images, indicative of myelin loss and gliosis (scarring).

There is no specific cure for CPM. Treatment is primarily supportive and focuses on managing symptoms and preventing complications. Measures may include:

• Monitoring: Close monitoring of electrolyte levels, especially sodium, to prevent rapid fluctuations.
• Symptomatic Treatment: Addressing specific symptoms such as dysphagia with speech therapy and physical therapy for muscle weakness.
• Prevention: Avoiding overly rapid correction of hyponatremia, particularly in high-risk individuals.

The prognosis of CPM can vary widely depending on the severity of the initial injury and the extent of neurological deficits. Some individuals may experience partial recovery of function with supportive care, while others may have persistent neurological impairments.

In summary, Central Pontine Myelinolysis (CPM) is a neurological disorder characterized by the destruction of myelin in the central pons, often due to rapid changes in serum sodium levels. It leads to severe neurological

Question 91

Focal weakness lasting for 24 hours following a motor seizure

Answer 91

postictal paralysis (Todd)

Question 92

symmetric upper non sensory motor neuron pattern of weakness involving the face, arm, and leg.

Answer 92

Pure motor stroke
Internal capsule

Question 93

most common type of
lacunar stroke

Answer 93

Pure motor stroke

Question 94

Px following MVA alert on hospital arrival loses consciousness when taking tests + pupil dilation + contralateral hemiparesis

Answer 94

epidural hematoma

Question 95

tear of the middle meningeal artery

Answer 95

epidural hematoma

Question 96

impaired walk along a straight line touching the heel of one foot to the toe of the other

Answer 96

Tandem gait
Cerebellar dysfunction

Tandem gait, also known as heel-to-toe walking, is a specific type of gait assessment used in neurological examinations to evaluate cerebellar function and balance. Here’s how it relates to cerebellar dysfunction:

During tandem gait assessment, the individual is asked to walk in a straight line placing one foot directly in front of the other, with the heel of the front foot touching the toes of the back foot on each step. This narrow base of support challenges balance and requires intact coordination and proprioception, both of which are functions primarily controlled by the cerebellum.

The cerebellum plays a crucial role in motor coordination, precision, and timing of movements. When there is dysfunction or damage to the cerebellum, such as from stroke, tumor, multiple sclerosis, or other neurological conditions, it can affect tandem gait in several ways:

1. Ataxia: Cerebellar ataxia is characterized by uncoordinated movements, including difficulty with tandem gait due to impaired balance and coordination.
2. Intention Tremor: Tremors that worsen with movement, which can affect the precision needed for heel-to-toe walking.
3. Dysmetria: Difficulty estimating the range or trajectory of movements, leading to overshooting or undershooting steps during tandem gait.
4. Dysdiadochokinesia: Impaired ability to perform rapid alternating movements, which may affect the ability to transition smoothly from one step to the next in tandem gait.

In a neurological examination, abnormal tandem gait can indicate cerebellar dysfunction or other neurological impairments affecting balance and coordination. The assessment helps clinicians localize the lesion (if present) and understand the severity of the impairment.

• Normal Tandem Gait: The ability to perform tandem gait without significant difficulty suggests intact cerebellar function and balance.
• Abnormal Tandem Gait: Difficulties in performing tandem gait, such as swaying, stepping off the line, or needing assistance for balance, may indicate cerebellar dysfunction or other neurological deficits.

Tandem gait is a simple yet effective test used in neurological examinations to assess cerebellar function and balance. It involves walking heel-to-toe in a straight line, challenging the coordination and proprioception controlled by the cerebellum. Abnormal tandem gait can suggest cerebellar dysfunction, aiding clinicians in diagnosis and treatment planning for various neurological conditions affecting motor coordination and balance.

Question 97

poor naming ability + non-fluent

Answer 97

Transcortical motor aphasia

Transcortical motor aphasia is a type of non-fluent aphasia characterized by difficulty in speech production despite relatively preserved comprehension and repetition abilities. Here are key features and characteristics of transcortical motor aphasia:

1. Speech Output Impairment: Individuals with transcortical motor aphasia struggle with initiating speech and producing fluent sentences. They may experience halting speech, speech fragmentation, and difficulty finding the right words (anomia).
2. Grammatical Errors: Speech may be telegraphic or agrammatic, lacking in grammatical structure and often limited to short phrases or single words.
3. Preserved Comprehension: Despite difficulties with speech output, comprehension of spoken and written language is relatively intact. Patients can understand verbal instructions and conversations to a significant extent.
4. Repetition Ability: Repetition of words and phrases is typically preserved or only mildly impaired. Patients can repeat words or sentences accurately, which distinguishes transcortical motor aphasia from other forms of non-fluent aphasia where repetition is more severely affected.
5. Fluency Variability: Speech fluency can vary depending on the context and level of support provided. In some cases, patients may experience greater fluency when using automatic speech or in more familiar situations.
6. Associated Motor Deficits: Sometimes, there may be associated mild or moderate limb weakness or apraxia (difficulty with motor planning), reflecting involvement of cortical areas beyond just language production regions.

Transcortical motor aphasia is typically caused by lesions in the frontal lobe of the dominant hemisphere of the brain, particularly in the supplementary motor area (SMA) or the precentral gyrus. Common causes include:

• Stroke: Ischemic or hemorrhagic strokes affecting the frontal lobe, often due to vascular occlusion or rupture.
• Traumatic Brain Injury: Injuries to the head or brain that result in focal damage to the frontal cortex.
• Brain Tumors: Tumors located in or near the frontal cortex can compress or invade language areas, leading to aphasia.

Diagnosis of transcortical motor aphasia involves a comprehensive neurological examination, including assessment of speech production, comprehension, repetition, and other cognitive functions. Imaging studies such as MRI or CT scans may be performed to identify the location and extent of brain lesions.

• Speech Therapy: Intensive speech and language therapy aimed at improving speech production, enhancing word-finding abilities, and optimizing communication strategies.
• Augmentative and Alternative Communication (AAC): Use of communication aids and strategies (e.g., picture boards, electronic devices) to facilitate communication.
• Supportive Care: Providing a supportive environment that encourages communication and understanding.

Prognosis for transcortical motor aphasia varies depending on the underlying cause, extent of brain damage, and individual response to therapy. With appropriate rehabilitation efforts, some individuals may show improvement in speech fluency and communication abilities over time.

In summary, transcortical motor aphasia is characterized by impaired speech production despite preserved comprehension and repetition abilities. It results from lesions in the frontal lobe of the

Question 98

poor naming ability + non-fluent + poor repetition

Answer 98

Broca aphasia

Broca’s aphasia, also known as non-fluent aphasia or expressive aphasia, is a type of language disorder primarily characterized by difficulties in speech production and language fluency, while comprehension generally remains intact to some extent. Here are key features and considerations regarding Broca’s aphasia:

1. Impaired Speech Production: Individuals with Broca’s aphasia have difficulty forming words and sentences. Speech may be slow, effortful, and characterized by short, choppy phrases or telegraphic speech (lack of grammatical structure).
2. Limited Vocabulary: Anomia, or word-finding difficulty, is common. Patients may struggle to retrieve specific words or use general terms to compensate for their difficulty.
3. Articulation Problems: Speech may be characterized by distorted or effortful articulation, often accompanied by phonemic errors (substitution or mispronunciation of sounds).
4. Preserved Comprehension: Despite difficulties in speaking, comprehension of spoken and written language is generally intact to varying degrees. Patients can understand conversations and instructions.
5. Difficulty with Repetition: Repetition of words or phrases is typically impaired in Broca’s aphasia, although this deficit may vary depending on the severity of the condition.
6. Awareness of Deficits: Patients are often aware of their language difficulties and may experience frustration or emotional distress due to their impaired ability to communicate effectively.

Broca’s aphasia typically results from damage or lesions to the posterior portion of the frontal lobe in the dominant hemisphere of the brain, usually the left hemisphere in right-handed individuals. Common causes include:

• Stroke: Ischemic stroke affecting the middle cerebral artery, which supplies blood to the frontal lobe.
• Traumatic Brain Injury: Head trauma resulting in focal damage to the frontal cortex.
• Brain Tumors: Tumors in or near the frontal cortex can compress or invade language areas, leading to aphasia.

Diagnosis of Broca’s aphasia involves a comprehensive neurological evaluation, including:

• Language Assessment: Evaluation of speech production, comprehension, repetition, naming abilities, and reading and writing skills.
• Imaging Studies: MRI or CT scans may be used to identify structural abnormalities or lesions in the brain, helping to localize the area of damage.

Treatment of Broca’s aphasia focuses on improving communication abilities and functional outcomes:

• Speech Therapy: Intensive speech and language therapy aimed at improving speech production, word retrieval, and sentence formation.
• Augmentative and Alternative Communication (AAC): Use of communication aids and strategies (e.g., picture boards, electronic devices) to facilitate communication.
• Family and Caregiver Education: Providing education and support to family members and caregivers to enhance communication interactions.

Prognosis for Broca’s aphasia varies depending on the cause, extent of brain damage, and individual response to therapy. Some individuals may show improvement in language function with intensive therapy, while others may experience persistent difficulties.

In summary, Broca’s aphasia is a language disorder characterized by impaired speech production and language fluency, while comprehension is relatively preserved. It results from damage to the frontal lobe of the dominant hemisphere of the brain and requires comprehensive evaluation and targeted therapy to improve communication abilities and quality of life for affected individuals.

Question 99

upper torso stooped forward + shuffling feet + lost arm swing

Answer 99

Parkinsonian gait

Question 100

affected foot is raised higher than normal + brought down with a slap

Answer 100

Steppage gait

Question 101

painful + limited weight bearing leg

Answer 101

Antalgic gait

Antalgic gait refers to an abnormal walking pattern that develops as a response to pain, typically in the lower extremities. It is characterized by a shortened stance phase on the affected side or limb, as the individual tries to minimize weight-bearing on the painful area. Here are key features and considerations regarding antalgic gait:

1. Reduced Weight-Bearing: The affected limb spends less time in contact with the ground during the stance phase of walking. This reduces the amount of weight placed on the painful area, which helps to alleviate discomfort.
2. Shortened Stance Phase: The stance phase of the gait cycle (when the foot is in contact with the ground) is shortened on the affected side. This results in a quicker transition to the swing phase (when the foot is off the ground).
3. Limping: Antalgic gait often results in a noticeable limp, where the individual may favor the non-painful side or attempt to minimize movement of the painful limb.
4. Pain Behavior: The individual may exhibit protective behaviors such as guarding the painful area, grimacing, or holding the limb in a position that reduces pain.

Antalgic gait can be caused by various conditions that produce pain in the lower extremities, including:

• Musculoskeletal Injuries: Such as fractures, sprains, strains, or joint injuries affecting the hip, knee, ankle, or foot.
• Arthritis: Inflammatory conditions such as osteoarthritis or rheumatoid arthritis affecting the joints of the lower limbs.
• Infection: Osteomyelitis or septic arthritis can cause significant pain and lead to antalgic gait.
• Neurological Disorders: Conditions affecting the nerves or nerve roots supplying the lower extremities, such as radiculopathy or neuropathy.

Diagnosis of antalgic gait involves a thorough clinical evaluation, including:

• History: Detailed history of the onset, duration, and characteristics of pain, as well as any preceding trauma or medical conditions.
• Physical Examination: Assessment of gait pattern, observation of pain behaviors, palpation of the affected area to identify tender points, and evaluation of range of motion.
• Imaging: X-rays, MRI, or CT scans may be used to identify structural abnormalities, fractures, or joint pathology contributing to the pain.

Treatment of antalgic gait focuses on addressing the underlying cause of pain and optimizing mobility:

• Pain Management: Use of analgesic medications or anti-inflammatory drugs to alleviate pain and reduce inflammation.
• Physical Therapy: Exercises to improve strength, flexibility, and gait mechanics. Modalities such as ultrasound or electrical stimulation may also be used.
• Orthotic Devices: Supportive footwear, braces, or assistive devices (e.g., cane or walker) may be prescribed to reduce weight-bearing on the painful limb.
• Surgical Intervention: In cases where conservative measures fail to relieve pain, surgical intervention may be necessary to address structural abnormalities or repair injuries.

The prognosis for antalgic gait depends on the underlying cause and the effectiveness of treatment. Prompt diagnosis and appropriate management can often lead to improvement in pain symptoms and restoration of normal gait mechanics over time.

In summary, antalgic gait is an abnormal walking pattern characterized by reduced weight-bearing on the affected limb due to pain. It is a protective mechanism to minimize discomfort and is commonly seen in various musculoskeletal and neurological conditions affecting the lower extremities. Treatment focuses on addressing the underlying cause of pain and optimizing mobility through pain management, physical therapy, and sometimes surgical intervention.

Question 102

Post stroke + stiff leg + foot drop+ flexed/adducted hand

Answer 102

Spastic hemiparetic gait

A spastic hemiparetic gait is a type of walking pattern seen in individuals who have weakness and stiffness (spasticity) on one side of their body. In simple terms, it looks like this:

• Spastic: Muscles are stiff and tight.
• Hemiparetic: Weakness affecting one side of the body.
• Gait: The way someone walks.

When someone has a spastic hemiparetic gait, they might drag one leg or swing it in a semicircle from the hip (circumduction) while walking. The affected arm on the same side might also be held close to the body with the elbow bent. This type of gait is often seen in conditions like stroke or cerebral palsy.

Question 103

short steps + extended stiff legs crossing on each other+ foot dragging

Answer 103

Spastic diplegia gait/ scissor gait

Question 104

abrupt onset of right face and hand weakness +
disturbed speech production, + a right homonymous hemianopsia

Answer 104

Left middle cerebral artery occlusion

Question 105

young female + weakness after exertion + Diplopia/Ptosis + chewing weakness

Answer 105

myasthenia gravis

Question 106

Severe myasthenia gravis treatment

Answer 106

Corticosteroids (prednisone)

Question 107

fluctuating level of consciousness + trivial force

Answer 107

Subdural hematoma

Question 108

head trauma + no loss of consciousness + deteriorating a few hours/days later

Answer 108

epidural hematoma

Question 109

Visual hallucinations + Parkinsonism +
+Fluctuation in the mental state

Answer 109

Lewy body dementia

Question 110

A headache exacerbated by coughing, sneezing or straining

Answer 110

brain tumours and raised intracranial pressure

red flag

Question 111

TIA 1st line treatment

Answer 111

Aspirin + dipyridamole

Question 112

Contraceptive pills + headache nausea and vomiting + Visual obscuration

Answer 112

Benign intracranial hypertension

Question 113

stroke secondary prevention medication

Answer 113

Warfarin
Aspirin
Enalapril
Atorvastatin

Question 114

symptoms which can aggravate dementia

Answer 114

-Depression.
-Subdural haematoma.
-Neoplasms.
-Alcohol.
-Intracerebral lesions (tumour, normal pressure hydrocephalus).
-Infections (urinary tract, respiratory tract)

Question 115

sudden, brief and very severe + paroxysms of pain + no sensory loss in the painful area + does not awaken + from
sleep

Answer 115

trigeminal neuralgia

Trigeminal neuralgia (TN) is a chronic pain condition affecting the trigeminal nerve, which is responsible for sensation in the face and controlling the muscles involved in chewing. Here are the key characteristics and features of trigeminal neuralgia:

1. Episodic, Severe Pain: Trigeminal neuralgia is characterized by sudden, intense, stabbing or electric shock-like pain in the areas of the face innervated by the trigeminal nerve. The pain episodes are typically brief but can be excruciatingly severe.
2. Location: The pain usually affects one side of the face, commonly around the eyes, nose, lips, forehead, and jaw. It rarely crosses to the opposite side of the face.
3. Trigger Factors: Pain episodes can be triggered by seemingly benign stimuli or activities, such as touching the face lightly, chewing, talking, brushing teeth, or exposure to cold air.
4. Paroxysmal Nature: The pain comes in paroxysms (sudden attacks) and may occur in clusters or bouts, followed by periods of remission where no pain is experienced.
5. No Sensory Loss: Unlike other conditions, there is typically no sensory loss or numbness in the affected areas between the episodes of pain.
6. Impact on Quality of Life: Trigeminal neuralgia can significantly impair daily activities, including eating, talking, and social interactions, due to the fear of triggering pain.

The exact cause of trigeminal neuralgia is often unknown, but it is thought to result from compression or irritation of the trigeminal nerve root near the brainstem. Possible causes include:

• Compression: Pressure on the trigeminal nerve by a blood vessel (most commonly the superior cerebellar artery) or a tumor.
• Demyelination: Damage to the myelin sheath of the trigeminal nerve, often associated with conditions like multiple sclerosis.

Diagnosis of trigeminal neuralgia is primarily based on clinical presentation and history. Imaging studies such as MRI may be performed to rule out structural causes or vascular compression of the trigeminal nerve.

Treatment of trigeminal neuralgia aims to relieve pain and improve quality of life. Options include:

• Medications: Anticonvulsant drugs such as carbamazepine or oxcarbazepine are commonly used to reduce nerve sensitivity and pain intensity.
• Surgical Procedures: For cases resistant to medication, surgical options like microvascular decompression (MVD), stereotactic radiosurgery (Gamma Knife), or percutaneous procedures (such as glycerol injection or radiofrequency ablation) may be considered to alleviate nerve compression or irritation.
• Supportive Care: Counseling, support groups, and pain management strategies can help individuals cope with the physical and emotional impact of trigeminal neuralgia.

The prognosis for trigeminal neuralgia varies. Some individuals experience periods of remission or respond well to medication or surgical interventions, while others may have persistent or recurrent symptoms despite treatment.

In summary, trigeminal neuralgia is a painful condition characterized by sudden, severe facial pain episodes, often triggered by routine activities. Prompt diagnosis and appropriate management are essential to relieve pain and improve quality of life for individuals living with this challenging neurological disorder.

Question 116

trigeminal neuralgia treatment

Answer 116

1st line: Carbamazepine
2nd line: Gabapentin and amitriptyline

Trigeminal neuralgia is a condition that causes sudden, severe facial pain. It feels like an intense, electric shock and usually affects one side of the face. The pain is triggered by everyday activities like brushing teeth, chewing, or even a light touch to the face. It occurs because of irritation or damage to the trigeminal nerve, which carries sensation from the face to the brain.

Question 117

feeling detached/unreal surroundings/deja vu + occasional headaches

Answer 117

Temporal lobe epilepsy

Question 118

lumbar puncture contraindications

Answer 118

– Unstable patient.
– Altered level of consciousness
– Space occupying lesion in the brain.
– Localised infection in the lumbar region.
– Coagulopathy (High INR)

Question 119

BPPV investigation

Answer 119

Hallpike manoeuvre

Question 120

BPPV treatment

Answer 120

Epley manoeuvre

Question 121

Meniere’s disease treatment

Answer 121

Frusemide

Question 122

Vestibular neuritis treatment

Answer 122

Steroids

Question 123

Epileptic px planning to conceive + seizure free 2 years

Answer 123

Gradually cease anti-epileptic over 6 months

Question 124

partial seizures 1st line treatment

Answer 124

Carbamazepine

Question 125

Horner’s syndrome + nystagmus + facial sensory deficit + side of the body sensory deficit

Answer 125

• posterior inferior cerebellar artery infarct (PICA)
• lateral medullary syndrome (Wallenberg syndrome)

Question 126

contralateral hemiparesis + contralateral homonyms hemianopia + aphasia + sensory neglect

Answer 126

middle cerebral artery lesion (MCA)

Question 127

generalized
tonic–clonic seizures + right eye swelling + testis tenderness + well-defined cystic lesions on cerebral cortex

Answer 127

Neurocysticercosis (tape worm)

Question 128

Absolute contraindications to thrombolytics therapy

Answer 128

• Uncertainty about the time of stroke onset (e.g. patients awakening from sleep).
• Neurologic surgery, serious head trauma, or previous stroke in past 3 months.
• Hypertension: systolic blood pressure above 180mmHg; or diastolic blood
  pressure above 110mmHg on repeated measures.
• Clinical presentation suggestive of subarachnoid haemorrhage even if the CT scan is normal.
• History of intracranial haemorrhage.
• Seizure at stroke onset.
• Suspected/confirmed endocarditis

Question 129

Trigeminal neuralgia vs post-herpetic neuralgia

Answer 129

history of herpes zoster eruption
trigeminal neuralgia involves a young person > 40

Question 130

adolescent with mild dementia+ tremor, + rigidity + acutely agitated + has jerking limbs when on l-dopa

Answer 130

Huntington disease

Question 131

Acute loss of peripheral vision + constricted pupils

Answer 131

concussion

Acute loss of peripheral vision along with constricted pupils can indicate a serious head injury, such as a concussion. Here’s a simple breakdown:

• Acute loss of peripheral vision: This means a sudden reduction in the ability to see things to the side while looking straight ahead. It can suggest damage to the optic pathways or the brain.
• Constricted pupils: Pupils that are smaller than normal and do not dilate properly in low light. This can be a sign of neurological impairment.

When these symptoms appear together after a head injury, it may indicate significant brain trauma or concussion, and immediate medical evaluation is necessary.

Question 132

ventriculoperitoneal shunting for NPH major complication

Answer 132

Subdural hematoma

Ventriculoperitoneal (VP) shunting is a common surgical treatment for Normal Pressure Hydrocephalus (NPH). While it can be highly effective, there are several potential complications associated with the procedure. The major complications include:

1. Shunt Malfunction: This is one of the most common complications and can occur due to blockage, disconnection, or breakage of the shunt components. Blockages can occur either in the ventricular catheter, the valve, or the peritoneal end of the shunt.
2. Infection: Shunt infection can occur, with symptoms ranging from fever, redness along the shunt path, abdominal pain, or neurological decline. Infection rates are higher in the initial months following surgery but can occur at any time.
3. Subdural Hematoma or Hygroma: Over-drainage of cerebrospinal fluid (CSF) can lead to the brain shifting within the skull, potentially causing tearing of bridging veins, leading to a subdural hematoma (bleeding) or hygroma (collection of CSF).
4. Abdominal Complications: These include pseudocyst formation, bowel perforation, and peritonitis, which can occur due to the presence of the shunt catheter in the peritoneal cavity.
5. Seizures: Although less common, seizures can occur postoperatively, potentially due to changes in intracranial pressure or the surgical procedure itself.
6. Mechanical Complications: These can include catheter migration, disconnection, or coiling, which may result in inadequate CSF drainage.

For more detailed information, you can refer to sources such as the National Institute of Neurological Disorders and Stroke or specific neurosurgery guidelines.

Question 134

abdominal aortic aneurysm repair + nilateral flaccid paresis + mpaired pinprick sensation

Answer 134

Spinal cord infarct

An abdominal aortic aneurysm repair can sometimes lead to complications such as a spinal cord infarct. In this context:

• Unilateral flaccid paresis: This refers to weakness on one side of the body, often affecting the lower extremities (legs), resulting in difficulty moving that side.
• Impaired pinprick sensation: This indicates a loss of sensation in response to sharp stimuli (like a pinprick) on one side of the body.

These symptoms together suggest damage to the spinal cord, specifically due to a spinal cord infarct. A spinal cord infarct occurs when the blood supply to the spinal cord is disrupted, leading to tissue damage and neurological deficits such as weakness and sensory loss.

In the scenario of an abdominal aortic aneurysm repair, complications like thromboembolism or hypoperfusion can potentially cause a spinal cord infarct due to compromised blood flow to the spinal cord. Immediate medical attention is necessary to manage this serious complication.

Question 135

progressive weakness + horizontal nystagmus horizontal nystagmus +ataxia + hyperreflexia + altered mental status

Answer 135

Phenytoin toxicity

Question 136

corneal abrasion + lack of eye pain

Answer 136

Trigeminal (CN) V lesion
- herpes zoster

Question 137

(in epidural hematoma)uncal herniation in temporal lobe causes:

Answer 137

• Ipsilateral fixed and dilated pupil from compression of the ipsilateral
  oculomotor nerve (CN III)
• Contralateral hemiparesis Contralateral hemiparesis (compression of the ipsilateral cerebral peduncle)

-Contralateral homonymous hemianopsia with macular sparing from
compression of the ipsilateral posterior cerebral artery

worsening herniation = psilateral hemiparesis, a false localizing sign known as Kernohan phenomenon

Question 138

pregnant + obese + papilledema + Pulsatile tinnitus + positional headaches positional headaches worse when lying flat

Answer 138

Idiopathic intracranial hypertension (IIH)

Question 139

head injury to the left temporal region + unresponsive after a lucid interval + progressive right-sided weakness

Answer 139

epidural hematoma

features Rapid expansion of the EH:
- Increase intracranial pressure (eg, Cushing
-triad of hypertension, bradycardia, and bradypnea),
- compress compress the temporal lobe leads to uncal herniation

Question 140

Idiopathic intracranial hypertension (IIH) investigation

Answer 140

MRI

Question 142

linear growth + pubertal delay, + worsening headaches + papilledema

Answer 142

craniopharyngioma
calcified suprasellar mass

Craniopharyngioma is a rare type of benign (non-cancerous) brain tumor that typically occurs near the pituitary gland, located just above the sella turcica (a bony structure at the base of the brain). This area is referred to as the suprasellar region.

1. Location:
   
   • Craniopharyngiomas are usually found in the suprasellar region, which is above the pituitary gland.
2. Calcification:
   
   • These tumors often contain calcium deposits, which can be seen on imaging tests like a CT scan. When doctors see a calcified suprasellar mass on a scan, craniopharyngioma is one of the conditions they consider.
3. Symptoms:
   
   • Because of their location, craniopharyngiomas can cause symptoms by pressing on nearby structures in the brain, such as:
     
     • Vision problems (due to pressure on the optic nerves).
     • Hormonal imbalances (affecting growth, metabolism, and more, due to pressure on the pituitary gland).
     • Headaches (from increased pressure in the brain).
     • Hydrocephalus (buildup of fluid in the brain due to blocked pathways).
4. Diagnosis:
   
   • The presence of a calcified mass in the suprasellar region on imaging is a key clue. MRI and CT scans are often used to diagnose craniopharyngioma.
5. Treatment:
   
   • Treatment typically involves surgery to remove the tumor, often followed by radiation therapy to target any remaining tumor cells.

• Craniopharyngioma: Think “cranium” (head) and “pharynx” (throat area) to remember it’s near the base of the brain.
• Calcified suprasellar mass: Imagine a “hard, rocky” (calcified) lump sitting “above the sella” (pituitary gland) in the brain.

This way, if you see the term “calcified suprasellar mass,” you can connect it with craniopharyngioma, a tumor near the pituitary gland that often contains calcium.

Question 143

craniopharyngioma location

Answer 143

suprasellar region adjacent to the optic chiasm

Question 144

hemineglect syndrome lovation

Answer 144

ipsilateral parietal cortex

Question 145

most common risk factor of stoke in young patients

Answer 145

Patent foramen ovale

Question 146

shoulder-tip pain ddx

Answer 146

• ectopic pregnancy
• Pulmonary embolism
  Pneumothorax
  Myocardial infarction
  Perforation of peptic ulcer disease
  Diaphragmatic irritation

Question 147

Parkinson’s disease vs Atypical parkinsonism

Answer 147

Parkinson’s disease:
- dramatic response to anti-cholinergics
- diplopia while reading
-autonomic dysfunction (constipation, urinary urgency, impotence, orthostasis?

Atypical parkinsonism:
- absence of response to high-dose levodopa
- absence of tremor