Neuro Flashcards
What is neurosyphilis, and what are its characteristics?
Answers:
🧠 Neurosyphilis is the invasion of the Central Nervous System (CNS) by Treponema pallidum, causing an inflammatory reaction.
💥 It affects the meninges, surrounding vessels, and cerebral parenchyma.
🤒 Acute aseptic meningeal syphilis presents with symptoms of acute meningitis, including neck stiffness and nausea.
💔 Meningovascular syphilis may lead to subacute strokes and cranial neuropathies.
»»»🤔 Think of neurosyphilis when there is a combination of stroke, rash, and meningitis symptoms.«««
> Meningovascular syphilis: subacute stroke + cranial neuropathies
What diagnostic investigations are used for neurosyphilis?
🧪 The Venereal Disease Research Laboratory (VDRL) test is especially useful in evaluating neurologic involvement by examining cerebrospinal fluid.
✅ In neurosyphilis, VDRL is positive in approximately 80% of patients.
🚫 However, it’s important to note that a false-positive VDRL result can occur in conditions such as pregnancy, viral infections (EBV, hepatitis), autoimmune diseases like lupus, leprosy, and some medications (e.g., chlorpromazine).
How is neurosyphilis managed and treated?
💉 IV Penicillin is the primary treatment for neurosyphilis and should be administered for 10-14 days at a dose of 18-24 million units per day, divided into 3-4 doses.
🚫 In cases of penicillin allergy, alternative treatments include doxycycline (100 mg orally twice a day for 28 days) or ceftriaxone (2 g daily intravenously for 10-14 days).
What are the key characteristics of Tabes Dorsalis (syphilitic myelopathy)?
🧠 Mnemonic: “DORSALIS” summarizes key features:
🔍 Dorsal column degeneration.
🦴 Orthopedic pain, leading to Charcot joints.
🚫 Reflexes decreased or absent deep tendon reflexes.
🩸Shooting pain or Dysesthesias: loss of sensation, particularly in the lower extremities, with sharp, shooting pain in the legs.
👀 Argyll Robertson pupil: bilateral miosis (constricted pupils) where pupils accommodate but do not react to direct or indirect light.
🚶♂️Locomotor ataxia / Progressive sensory broad-based ataxia, often leading to gait disturbances.
🧪 Syphillis
What are the clinical symptoms associated with elevated intracranial pressure (ICP)?
🫁 Cushing triad: irregular breathing (Cheyne-Stokes, Low blood pressure (wide pulse pressure), bradycardia.
😴 Reduced level of consciousness.
🤕 Headache.
🤢 Vomiting.
👁️ Papilloedema (optic disc swelling).
👓 Diplopia (double vision).
What are the neurological symptoms associated with hypercapnia due to respiratory failure?
🫁 Shortness of breath.
🤕 Headaches.
😴 Persistent tiredness or sluggishness during the day.
🤷♂️ Disorientation.
🤪 Confusion or altered mental state.
🤯 Paranoia.
😞 Depression.
⚡ Seizures.
What are the clinical symptoms associated with epidural hematoma?
🧠 Initial loss of consciousness immediately following a head injury.
🤔 Temporary recovery of consciousness with a return to normal or near-normal neurological function (lucid interval).
🫁 Signs of raised Intracranial Pressure (ICP), including headache and Cushing triad (irregular breathing, wide pulse pressure, bradycardia).
🧯 Cerebral herniation: acutely worsening level of consciousness, pupillary changes, new focal neurological deficits (e.g., hemiparesis, decerebrate posturing), and cardiorespiratory compromise (bradycardia, apnea).
— 👁️ Uncal herniation: 3rd nerve (oculomotor) nerve palsy causing a fixed dilated pupil and the eye “out and down.”
Clinical Features of PICA (Posterior Inferior Cerebellar Artery) Infarction Leading to Lateral Medullary Syndrome
🚶♂️ Ataxic gait (broad-based gait) and nystagmus (involuntary eye movements).
👁️ Ipsilateral Horner syndrome, characterized by ptosis (drooping eyelid), miosis (constricted pupil), and anhidrosis (lack of sweating) on the affected side of the face.
😣 Ipsilateral loss of facial sensation to pain and temperature sensation.
💔 Contralateral loss of pain and temperature sensation of the body (on the opposite side).
🧤 Dissociated anesthesia: Loss of pain and temperature sensation with spared proprioception, light touch, and vibration sense (lesion below the pons).
🌀 Vertigo, difficulty with swallowing, dysarthria (speech difficulty), and hoarseness (IX, VIII and X impairment).
Main features of infarction in:
Anterior cerebral artery
Middle cerebral artery
Posterior communicating artery
PICA
👣 Anterior Cerebral Artery infarction often presents with LOWER LIMB impairment. Contralateral paresis, sensory loss legs > arms.
🚽 Urinary incontinence may occur.
🧠 Executive function impairment, affecting decision-making, planning and other higher cognitive functions can be observed. Also personality change (disinhibition, abulia).
Main features of infarction in:
Middle cerebral artery
😶 FACE ASYMMETRY is a common feature, often presenting as facial droop.
🖐️ Upper limbs may be affected, and there might be some involvement of the lower limbs.
🚗 Middle Cerebral Artery infarctions are often related to occlusion in the internal carotid artery.
Main features of infarction in:
Posterior communicating artery AND
PICA
Posterior Communicating Artery
🤕 Severe pain and headache can be prominent symptoms.
👁️ Ocular palsy may occur, affecting eye movement.
Posterior Inferior Cerebellar Artery (PICA)
👁️ Horner Syndrome is often observed in PICA infarctions, characterized by ptosis, miosis, and anhidrosis on the affected side of the face.
🚶♂️ PICA infarction may lead to gait and coordination problems, including ataxia (uncoordinated movements) and difficulty walking.
🙁 Facial weakness or paralysis may occur, affecting muscles on one side of the face.
🚫 Dysphagia (difficulty swallowing) can be a symptom.
🌪️ Vertigo and dizziness may be prominent, along with nausea and vomiting.
👁️ Nystagmus (involuntary eye movements) may also be observed.
🧠 Other possible features include limb weakness, sensory deficits, and Horner syndrome (ptosis, miosis, anhidrosis).
What are the key principles in the management of acute stroke?
⏱️ Early intervention is crucial within 3-4.5 hours of onset with tissue plasminogen activator (tPA) such as alteplase administered intravenously or tenecteplase.
🚫 Aspirin should be withheld for the first 24 hours in some cases.
💊 Aspirin (150-300 mg orally) can be initiated within 48 hours if tPA is not used.
🩺 Hypertension should be treated if the blood pressure is elevated (>200/120 mmHg).
☎️ Contact a local neurological center if surgery is required, such as intracerebral hemorrhage for surgical clot extraction or evidence of raised intracranial pressure for decompression.
💊 Clopidogrel 75 mg is used for dual therapy (in combination with aspirin) in transient ischemic attack (TIA) within 24 hours.
What is the management and the recommended investigations for a Transient Ischemic Attack (TIA)?
⏰ TIA typically presents with a sudden onset and short duration (less than 60 minutes).
⚖️ Complete clinical recovery occurs in less than 24 hours, usually within 2 hours, and consciousness is usually preserved.
What investigations are recommended for evaluating a Transient Ischemic Attack (TIA)?
🧠 The next step in evaluation is often a CT scan without contrast.
📊 An MRI is the preferred imaging modality (within 24 hours if available), especially in cases of suspected brain stem ischemia.
🚗 Duplex Doppler ultrasound of the carotid arteries is advisable if there is a carotid bruit or a history of amaurosis fugax (transient monocular blindness) or anterior circulation involvement. This should be done within 48-72 hours.
🫀 Additional investigations may include a 12-lead ECG/Holter and echocardiogram (ECHO), especially if there are signs of atrial fibrillation (AF), acute myocardial infarction (MI), endocarditis, or posterior circulation involvement.
What are the clinical features associated with myelopathy at the C5-C6 level?
🤷♂️ Lower Motor Neuron (LMN) signs are typically observed at the level of the lesion. These signs include flaccid weakness in the upper extremities and muscle wasting.
🚶♂️ Upper Motor Neuron (UMN) signs are present below the level of the lesion, resulting in a spastic gait with stiffness and the presence of Babinski’s sign.
🤖 Sensory symptoms such as numbness and tingling in the arms are less common.
🏥 Autonomic symptoms may include bowel and bladder incontinence, as well as erectile dysfunction.
Differential diagnosis of myelopathy at c5-6
Motor neuron disease gives UMN and LMN signs, but there is no the level of compression. UMN and LMN symptoms will be seen on upper limbs as well as low limbs (assymetric). No sensory symptoms. The age of onset is young adults.
Multiple sclerosis motor (UMN lesion signs) and sensory symptoms, diffuse. Mean age of onset 30s plus visual symptoms.
Subacute combined degeneration of spinal cord can cause spastic paresis, but in addition there are impaired vibration, proprioception, ataxia, paresthesia plus anaemia.
Diabetic peripheral neuropathy LMN lesion signs (muscle wasting), symmetrical low limbs more than upper limbs, gloves and stocking distribution. Sensory symptoms (pin and needles).
What are the common investigations used in the diagnosis of Guillain-Barre Syndrome?
💉 Lumbar puncture is a key investigation, revealing albuminocytologic dissociation.
⚡ Nerve conduction studies are often performed to assess nerve function.
What are the recommended treatments and management strategies for Guillain-Barre Syndrome?
💉 Jg Intravenous immunoglobulin (IVIG) or plasmapheresis (plasma exchange) are often used as treatments.
🫁 Monitoring of respiratory function is crucial.
🫂 Mechanical ventilation should be considered if there are signs of respiratory failure.
What are the clinical features commonly associated with Multiple Sclerosis (MS)?
Young age
Useless hand due to loss of position sense, incoordination.
Dysmetria – lack of accuracy in voluntary movements.
Intention tremor (cerebellar involvement).
UMN lesion (pronator drift due to difference in muscle tone).
Sensory impairment regional.
What investigations are commonly used in the diagnosis and evaluation of Multiple Sclerosis (MS)?
🧲 MRI with contrast is an important tool, revealing contrast-enhancing lesions in more than one part of the central nervous system (CNS).
💉 Lumbar puncture may show elevated levels of IgG.
👁️ Visual evoked potentials are often performed and may reveal delayed responses.
How is Multiple Sclerosis (MS) typically managed and treated?
💉 Acute relapses may be treated with intravenous methylprednisolone for 3 days.
⚗️ In some cases, plasma exchange may be considered if the patient is unresponsive to treatment.
💊 Disease-modifying treatments include interferon, glatiramer acetate, and natalizumab.
🩺 Other treatments may involve medications like baclofen, clonazepam, oxybutynin, and carbamazepine.
What are the key differences in the presentation of facial paralysis between cerebral infarction involving the corticobulbar tract and Bell’s palsy?
🔴 In cerebral infarction involving the corticobulbar tract, only the lower two-thirds of the face is affected (UMN-type lesion), and the forehead is not affected. The person can fully raise their eyebrow.
🟡 In Bell’s palsy, which affects the 7th cranial nerve (LMN-type lesion), the entire ipsilateral half of the face is affected. The individual cannot fully raise the eyebrow and may have difficulty closing the eye.
What are some of the common side effects associated with donepezil and other cholinesterase inhibitors?
🩸 Sweating
🤤 Excessive salivation
😢 Increased lacrimation (tear production)
💦 Frequent urination
💩 Diarrhea
🍽️ Anorexia (loss of appetite)
🤢 Nausea
🤮 Vomiting
🧩 Excitation of neuromuscular function
👁️ Miosis (constricted pupils)
💪 Muscle spasms
🫁 Bronchospasm
🫀 Bradycardia (slow heart rate)
What are the clinical features commonly associated with Lewy Bodies Dementia?
👁️ Visual hallucinations are a notable symptom.
🚶 Parkinsonism, characterized by movement problems similar to Parkinson’s disease, may be present.
🧠 Dementia is a key component, with deficits in executive function and memory loss being prominent.
💤 REM sleep disorder is often observed, leading to disturbances during rapid eye movement (REM) sleep.
What are the key steps in managing agitated delirium?
👥 Nonpharmacological measures should be the initial approach, including providing supportive care and reassurance.
🩺 Identify and treat any easily reversible causes of delirium, such as dehydration, pain, hypoxia, or urinary retention.
🗣️ Engage in calm verbal interaction with clear communication to help manage agitation.
🚫 Avoid the use of physical restraints whenever possible.
💊 If nonpharmacological measures are insufficient and the delirium is refractory, medications such as Haloperidol, Olanzapine, or Risperidone may be considered.
🍷 In cases of delirium due to alcohol withdrawal, benzodiazepines like Lorazepam may be appropriate
What are the clinical symptoms and effects associated with carbamazepine toxicity?
🧠 In the central nervous system (CNS), symptoms may include ataxia, nystagmus, diplopia, dizziness, vertigo, sedation, drowsiness, coma, and seizures.
❤️ Cardiovascular system effects can manifest as tachycardia, hypotension, and potentially life-threatening arrhythmias, such as heart block, widening of QRS complex, and ventricular fibrillation.
🌼 Anticholinergic effects may result in urinary retention, decreased bowel motility, dry mouth, and sinus tachycardia.
💉 Bone marrow toxicity can lead to conditions like agranulocytosis and pancytopenia.
What are the guidelines for driving after seizures in various scenarios?
🚗 For individuals under treatment whose epilepsy was previously well controlled and had no seizures during the 12 months leading up to the last seizure, they can drive if they remain seizure-free for at least 3 months.
🚗 In the case of a first seizure of any type, driving is permitted if there are no further seizures (with or without medications) for at least 6 months.
🚫 During planned withdrawal of antiseizure medication, individuals should not drive while the dose is being tapered and for 3 months after the last dose.
🚗 If seizures recur after withdrawal, driving can be resumed if the previously effective medication is restarted, and there have been no seizures for 4 weeks.
What are the clinical features commonly associated with Guillain-Barré Syndrome (GBS) and its possible preceding infections?
🩸 GBS is characterized by an autoimmune attack on the peripheral nerves, particularly the myelin sheath.
🦠 Preceding infections are common triggers for GBS and can include Campylobacter jejuni, upper respiratory tract infections (URTI), Epstein-Barr virus (EBV), and cytomegalovirus (CMV).
🦠 GBS can be distinguished from conditions affecting different areas of the nervous system: anterior horn cells (motor neuron disease), dorsum spinal columns (subacute combined degeneration of spinal cord), central canal of spinal cord (syringomyelia), and neuromuscular junction (conditions like botulism and myasthenia gravis).
What are the clinical features and manifestations associated with radial nerve dysfunction, including “Saturday night palsy”?
💪 Radial Nerve Dysfunction, often referred to as “Saturday night palsy” or “Sleep paralysis,” can occur due to unintentional prolonged radial nerve compression, typically after alcohol or drug intoxication.
🔁 Posture-induced radial neuropathy is caused by entrapment of the radial nerve, which spirals around the humerus bone.
🦾 Radial Nerve Dysfunction can lead to weakness of the triceps muscle (elbow extension), weakness of wrist (wrist drop), and difficulty with finger extension. It may also result in numbness, paraesthesia, and pain along the lateral posterior arm.
What are some of the key features and conditions associated with nerve palsy, including posterior interosseous nerve, ulnar nerve, and median nerve dysfunction?
🖐️ Posterior Interosseous Nerve Dysfunction: Presents with weakness of finger extension.
👇 Ulnar Nerve Dysfunction: Characteristics include atrophy of hypothenar muscles, inability to flex the ring finger and little finger, claw hand deformity, inability to adduct the thumb, and persistent abduction of the little finger.
✋ Median Nerve Dysfunction: Features comprise loss of thumb opposition and abduction, loss of index and middle finger flexion (resulting in a “hand of benediction”), impaired wrist pronation and flexion, and atrophy of the thenar muscles.
What are the main divisions of the trigeminal nerve (CN V) and their functions?
Ophthalmic (upper) division: Innervates forehead 👩⚕️, upper eyelid 👁️, cornea 🌰, conjunctiva 🧴, dorsum of the nose 🐽, and anterior cranial fossa dura 🧠. It exits the orbit via the superior orbital fissure. Also associated with the trigeminal ganglion.
Maxillary (middle) division: Supplies upper lip 👄, lateral and posterior nose 👃, upper cheek 🥴, anterior temple 🏛️, upper jaw 👅, upper teeth 🦷, roof of the mouth 🏠, and middle cranial fossa dura 🧠. It exits through the foramen rotundum and passes through the cavernous sinus before entering the trigeminal ganglion.
Mandibular (lower) division: Provides sensation to the lower lip 👄, chin 😬, posterior cheek 🧏, temple 🏛️, external ear 🌂, lower mouth 👅, anterior two-thirds of the tongue 👅, and anterior/middle cranial fossa dura 🧠. Proprioceptive impulses mainly carried by the motor nerve. Enters the cranium via the foramen ovale and connects to the trigeminal ganglion.
What are the functions of the trigeminal nerve (CN V) divisions?
Ophthalmic division: Sensation from the forehead, upper eyelid, cornea, and related structures. Involved in the corneal reflex. 😲
Maxillary division: Provides sensation to the upper face, including the upper lip, nose, cheek, temple, and upper teeth. Also, dura innervation in the middle cranial fossa. 😷
Mandibular division: Supplies sensation to the lower face, chin, cheek, and tongue. Contains proprioceptive fibers for the muscles of mastication. Also, dura innervation in the anterior/middle cranial fossa. 😬
What autonomic functions are associated with the trigeminal nerve (CN V)?
Sympathetic and parasympathetic fibers: Join all three divisions of CN V and are responsible for various autonomic functions, including pupillary control 👁️, nasal mucosa mucus secretion 🤧, lacrimal gland function 😢, submaxillary gland function 😛, sublingual gland function 🤤, and arteriole control in the face 🩸.
What muscles are supplied by the motor division of CN V, and what are their functions?
Motor division supplies muscles for:
Elevation (Masseter, Temporal) 💪
Side-to-side movements (Pterygoid) ↔️
Depression (Mylohyoid, Digastric) 👇
Also, tensor tympani and tensor palati muscles are included. 🥁
Consequences of motor division lesions in CN V.
Lesions lead to:
Jaw muscle dysfunction (opening, chewing) 😬
Impaired mandible movements 🗣️
Atrophy in nuclear or infranuclear lesions. 🏋️♂️💔
Describe the jaw jerk reflex and clinical implications.
Jaw jerk reflex is a deep tendon or stretch reflex.
Normal response: Tapping the mandible produces a brisk contraction.
Abnormal response with upper motor neuron lesions: Hyperactive or repeating reflex (clonus) during jaw tapping.
Abnormal response with nuclear or infranuclear lesions: Absence of the reflex.
Clinical significance: Helps assess the integrity of the motor component of CN V and related neural pathways. 🧠⚙️
Which cranial nerves mediate the sense of taste and their respective areas?
Facial nerve (CN VII): Mediates taste in the anterior 2/3 of the tongue. 👅
Glossopharyngeal nerve (CN IX): Provides taste sensation in the posterior 1/3 of the tongue. 👅
Vagus nerve (CN X) (via superior laryngeal branch): Innervates taste buds in the laryngeal surface of the epiglottis. 🍽️
Trigeminal nerve (CN V): Provides general sensation to the tongue but not taste. No taste loss in CN V lesions. 🚫👅
What are the characteristics of third nerve palsy and its impact on vision?
Third cranial nerve (CN III) supplies:
Levator palpebrae muscle of the eyelid
Extraocular muscles: medial rectus, superior rectus, inferior rectus, inferior oblique 🚀
Functions of these muscles: Adduct, depress, and elevate the eye 👁️
Acute acquired third nerve palsy symptoms:
Sudden onset binocular diplopia
Droopy eyelid
Pupil reflex remains intact in ischemic palsies (e.g., due to diabetes or midbrain infarcts). 🩺 - The efferent limb of the III
What are the characteristics of fourth nerve palsy and its impact on vision?
Fourth cranial nerve (CN IV) palsy:
Binocular vertical diplopia 👓
Subjective tilting of objects (torsional diplopia)
Affected eye often extorted due to superior oblique muscle involvement (intorsion) 🔄
Challenges with down-gaze vision, like navigating stairs. 🏞️
Describe sixth cranial nerve (CN VI) palsy and its clinical findings.
CN VI palsy:
Isolated weakness of abduction of the affected eye 👀
Horizontal binocular diplopia 🎯
Examination findings:
Esotropia (inward deviation)
Worsened with gaze towards the affected lateral rectus muscle
Limited abduction on the affected side
Predisposing factor: Poorly controlled diabetes 🩺🍭
What are the clinical findings that suggest upper motor neuron (UMN) involvement?
Stiffness (spasticity) 💪
Brisk tendon reflexes (hyperreflexia) – unless concurrent lower motor neuron (LMN) involvement 🔄
Presence of abnormal reflexes (e.g., Babinski, Chaddock, or Hoffman signs) 🏥
Loss of dexterity despite normal strength 🤲
Muscle spasms 💥
What are the clinical findings indicative of lower motor neuron (LMN) dysfunction?
Twitching muscles (fasciculations) – often early manifestation, commonly seen in the tongue and limbs 👅💪
Reduction of muscle bulk (atrophy) 📉
Foot drop (or wrist drop in upper limb involvement) 🦶🤲
Depressed reflexes 📉
Breathing difficulties 🫁
How do electromyography (EMG) and nerve conduction studies (NCS) contribute to the diagnosis of ALS?
EMG and NCS are crucial for confirming the diagnosis of ALS and excluding peripheral conditions resembling ALS. ⚡️🩺
Some consider EMG/NCS as an extension of the physical examination. 👩⚕️📈
What are the challenges and diagnostic tools used in the diagnosis of ALS?
ALS diagnosis is primarily clinical, relying on appearance and neurologic examination findings, especially in advanced cases. 🧐👩⚕️
Diagnosis in early stages can be challenging due to nonspecific symptoms, requiring exclusion of other possible causes. 🤔
No pathognomonic test exists for ALS.
Often, several months (average 14 months) are needed for a definite diagnosis.
What is the role of imaging studies and lumbar puncture in ALS diagnosis?
Imaging studies (e.g., CT scan, MRI) are often used to assess other conditions (e.g., multiple sclerosis, spinal lesions) that can mimic ALS but are usually normal in ALS patients. 📷🧠
Lumbar puncture and examination of cerebrospinal fluid (CSF) are not necessary unless the patient presents with either pure upper motor neuron (UMN) or pure lower motor neuron (LMN) symptoms, ruling out other conditions. 🌡️🩸
What are the key characteristics and diagnostic considerations of ALS?
ALS is the most common adult-onset neurodegenerative disease, characterized by:
Progressive skeletal muscle weakness and wasting (amyotrophy)
Spasticity
Fasciculations
It affects both upper motor neurons (UMNs) and lower motor neurons (LMNs). 🦠🦴
ALS ultimately leads to respiratory paralysis. 🫁
A single area should exhibit abnormalities in both LMNs and UMNs to strongly suggest ALS as the diagnosis.
In 90-95% of cases, ALS is sporadic; only 5-10% are hereditary. 🧬🤝
What clinical features should raise suspicion of ALS as a diagnosis?
ALS should be suspected when there is:
Insidious loss of function
Gradual, slowly progressive, painless weakness in one or more regions of the body 🏃♂️🤔
No changes in sensation
No other explanation for the presentation 🧩
Over time, patients with ALS develop both LMN and UMN involvement. 👣🧠
What are the characteristic clinical features and symptoms of CTS?
Classic CTS presents with:
Pain and paresthesia in the distribution of the median nerve territory in the hand (first three digits and radial half of the fourth digit) 🖐️💤
Symptoms often worsen at night and may awaken patients. 🌙🛏️
Patients may use hand movements or warm water to alleviate symptoms. 🚿💆
Symptoms may be localized to the wrist or involve the entire hand, with possible radiation into the forearm, elbow, or shoulder. 🤔🦾
Activities involving wrist flexion/extension or arm raising can worsen symptoms. 📝🚗
What happens when there is a median nerve injury at the wrist?
Median nerve injury at the wrist causes weakness in the thenar eminence muscles: flexor pollicis brevis, abductor pollicis brevis, and opponens pollicis. These muscles are not involved in wrist extension. 🖐️
What are the consequences of a median nerve injury at the elbow?
Median nerve injury at the elbow results in dysfunction of all the muscles innervated by the median nerve and its motor branch, the anterior interosseous nerve. These include all muscles in the anterior compartment of the forearm, muscles of the thenar eminence, and the 1st and 2nd lumbrical muscles. However, wrist extension is not affected by median nerve injuries at the elbow. 🦾🦴
What occurs with a radial nerve injury at the wrist?
Radial nerve injury at the wrist does not cause motor function impairment but results in sensory deficit in the territory of the radial nerve, including the dorsal aspect of the thumb, index and middle fingers, the radial half of the ring finger, and the dorsal aspect of the first web space. 🤚🧤
What are the effects of ulnar nerve injury at the elbow?
Ulnar nerve injury at the elbow affects:
Flexion of fingers 4th and 5th
Wrist flexion (paralysis of the flexor carpi ulnaris muscle and radial deviation when flexion is attempted)
The 3rd and 4th lumbrical muscles
Interosseous muscles of the hand
Muscles in the hypothenar eminence 🤘👋
Sensory deficits in the territory of the ulnar nerve can also occur, but wrist extensor muscles remain unaffected by ulnar nerve injuries. 🧤🚫
What is Benign Paroxysmal Positional Vertigo (BPPV) and what are its common characteristics?
BPPV is characterized by recurrent acute attacks of vertigo, nausea, and vomiting, typically without tinnitus or hearing impairment. 🤢🌀
It can affect individuals of any age, including young and otherwise healthy individuals. 🙋♀️🧡
The condition is caused by an accumulation of calcium crystals in the posterior semicircular canal, disrupting the movement of endolymph and causing vertigo. 💎🔀
What are the classic symptoms and diagnostic maneuvers for BPPV?
Classic symptoms of BPPV include brief episodes of vertigo (usually lasting a few seconds), often accompanied by nausea and nystagmus. 🤮👀
Vertigo episodes are triggered by rapid changes in head position and may recur after remission. 🔄📅
Nystagmus observed in BPPV has a rotational pattern. 🌀
The Dix-Hallpike maneuver is used for diagnosing BPPV. 🩺
What is the Dix-Hallpike maneuver?
The Dix-Hallpike maneuver is a diagnostic test used to evaluate and diagnose Benign Paroxysmal Positional Vertigo (BPPV). 🩺🤔
During this maneuver, the patient is seated upright on an examination table, and the clinician assists the patient in lying down quickly with their head hanging over the edge and their neck extended. The clinician observes the patient’s eye movements for nystagmus and asks the patient about their experience of vertigo. 🛏️👁️
The presence of nystagmus and vertigo during specific head positions indicates a positive result for BPPV. Different head positions can help identify which semicircular canal is affected. 🌀👂
What is the Epley maneuver?
The Epley maneuver is a therapeutic maneuver used to treat Benign Paroxysmal Positional Vertigo (BPPV) by repositioning the dislodged calcium crystals in the semicircular canals to their normal position. 🛏️🔀
During the Epley maneuver, the patient is initially seated upright. The clinician guides the patient through a series of head position changes, starting with the affected ear down and ending with the head turned to the unaffected side and facing downward. Each position is held for a specific duration. This maneuver aims to move the calcium crystals out of the affected canal and into a less symptomatic position. 🔄👂
The Epley maneuver is often effective in alleviating the symptoms of BPPV. Multiple repetitions of the maneuver may be needed in some cases. 💪🔁
What is a cluster headache?
Cluster headache, also known as migrainous neuralgia, is characterized by severe, unilateral pain in the orbital, supraorbital, or temporal region, often accompanied by autonomic symptoms. 🤕👁️👃
Attacks of cluster headache can occur up to eight times a day and are relatively short-lived. The pain is extremely intense, and patients often exhibit restlessness during attacks. 💥😫
Unlike migraine headaches, cluster headaches are not associated with nausea and vomiting. However, they are often accompanied by autonomic symptoms such as ptosis, miosis, lacrimation, conjunctival injection, rhinorrhea, and nasal congestion. 🩺😢
How is a cluster headache typically treated?
The initial treatment for a cluster headache attack is 100% oxygen administered through a tightly-sealed face mask for 15 minutes. This can alleviate the headache in many patients. 🌬️😌
If oxygen therapy is ineffective, medications like Sumatriptan (intramuscularly or intranasally), Dihydroergotamine (intramuscularly), or Lidocaine (intranasally) may be considered. Nasal congestion can affect the effectiveness of intranasal medications. 💊👃
Once cluster headache is diagnosed, preventive treatment is initiated with verapamil (immediate release) as the first-line medication. Other options include Methysergide, corticosteroids, or lithium, although these are not the first choice due to associated complications. Methysergide, for example, can lead to retroperitoneal, cardiac, and/or pleural fibrosis. 🩹💊
Do not give a triptan for 24 hours after dihydroergotamine therapy!!!!!!!!
What’s the recommended verapamil dosage and special care for cluster headache treatment?
Immediate-release verapamil is considered more effective than sustained-release forms. 💊🕒
Recommended verapamil dosing:
Start with verapamil immediate-release 80 mg orally, three times daily for two weeks.
Then, increase to 120 mg three times daily for two weeks.
Finally, escalate to 160 mg three times daily.
ECG should precede each dose increase, and raising the dose should depend on a normal ECG. 📊🩺
However, it can lead to heart block, especially at higher doses, which may become evident up to 10 days after starting or increasing the dose. 🩺🚫
An initial electrocardiograph (ECG) is essential to rule out heart block, bradycardia, and prolonged PR interval. ECGs must be repeated before dose increases, and only if ECG results are normal should the dose be raised. 📈
What is subacute combined spinal cord degeneration in vitamin B12 deficiency?
Peripheral neuropathy + myelopathy
Clinical presentation: 🩸 Paresthesia, weakness, ataxia, 🧠 Neuropsychiatric symptoms
Distal paresthesia and extremity weakness are common initial complaints
Followed by spastic paresis and ataxia (positive Romberg test)
Physical exam reveals deficits in vibration and proprioception
Pyramidal signs include plantar extension and hyperreflexia
Ocular findings: 👁️ Scotoma, optic atrophy
Diagnosis: Measure serum vitamin B12 level
Treatment: 💊 Replacement of vitamin B12
ℹ️ Peripheral neuropathy + myelopathy = Subacute Combined Spinal Cord Degeneration (Vitamin B12 Deficiency)
What action should be taken if a patient with recent mild stroke or TIA has a high-grade ipsilateral carotid stenosis (≥70%)?
Screen for carotid stenosis in all patients with ischaemic stroke or TIA in the carotid circulation territory. Confirm with a second imaging test if necessary. 🧐
Urgently refer patients with high-grade ipsilateral carotid stenosis for carotid endarterectomy within 2 weeks for maximum benefit. Surgery’s benefit diminishes after 3 months or with 50-69% stenosis. ⏳
When is percutaneous transluminal cerebrovascular angioplasty and stenting considered for carotid stenosis?
Consider percutaneous transluminal cerebrovascular angioplasty and stenting for carotid stenosis in certain situations (e.g., high surgical risk due to technical challenges). 🏥
After carotid endarterectomy, implement intensive secondary prevention therapy, including antiplatelet drugs, blood pressure control, cholesterol management, and lifestyle changes (e.g., smoking cessation). 🚭
Which cerebral arteries would typically be implicated in a stroke within the carotid circulation territory?
Common cerebral arteries implicated include the middle cerebral artery (MCA) and anterior cerebral artery (ACA). 🧠
The internal carotid artery (ICA) supplies blood to the MCA and ACA. 💉
What is the most commonly injured lower extremity nerve in patients in the lithotomy position during surgery? What are the risk factors associated with this nerve injury?
The most commonly injured lower extremity nerve in this position is the common peroneal nerve, a branch of the sciatic nerve 🦵
Injury often occurs due to compression between the lateral aspect of the fibular head and the leg-holding bar, especially when using candy cane stirrups. 🍭
Risk factors include low patient weight, smoking, and prolonged surgery duration. ⚖️🚬⏳
Which presentation is most suggestive of sciatic nerve injury
Absent ankle reflex.
Also shown: paralysis of the hamstring muscles (knee flexion weakness) and all the muscles below the knee
Decreased sensation over the anterior thigh and medial leg is caused by which nerve injury?
Femoral nerve
What are the common symptoms associated with acoustic neuromas, and why is acute onset of unilateral hearing loss less likely?
Gradual hearing loss is the most common presenting symptom of acoustic neuromas. 🗣️
Acute onset of unilateral hearing loss is less likely (5-15% of cases). Deafness typically has an insidious onset in this condition. 🔉
Imbalance and vertigo are not prominent features because tumor growth disrupts vestibular nerve function slowly, allowing for compensation over time. 🤸♂️
Other features may include headache and facial sensory impairment. 🤕🧑⚕️
What is the most initial investigation to consider for a patient with sudden-onset decreased vision and retro-orbital pain?
Highly suggestive of optic neuritis (ON)?
The most initial investigation to consider for a patient with suspected ON is an MRI of the brain. 🧠
MRI is highly sensitive and specific in assessing inflammatory changes in the optic nerve, ruling out structural lesions, and predicting future development of multiple sclerosis (MS) in patients presenting with acute ON.
What are some additional diagnostic tools and considerations for patients with ON?
Visual evoked potentials (VEP) can provide a more sensitive diagnostic yield compared to MRI in ON, especially when MRI is negative or inconclusive. 📈
Temporal artery biopsy is not necessary for patients with suspected ON unless temporal arteritis is suspected based on age and symptoms. ❌
Lumbar puncture (LP) may be considered in patients with normal or atypical brain MRI findings, where CSF examination can reveal oligoclonal bands. 💉
Fundoscopy may not always reveal abnormalities in ON, especially in cases of retrobulbar ON. 🚫
Which nerve injury is associated with fractures of the humeral neck?
Radial nerve
Proximal radial nerve injuries can lead to wrist drop or decreased/absent thumb extension and abduction. 🖐️
Obs: Injury to the axillary nerve is associated with fractures of the humeral neck. 🦴
