Neurology Flashcards

1
Q

Describe the anatomy of common sites of nerve root compression (C6, C7, L5, S1)

A

Nerve root compression, also known as a radiculopathy, occurs when nerve roots exiting the spinal column are impinged or irritated by surrounding tissues such as bones, cartilage, muscles, or tendons. This condition can cause pain, weakness, or numbness in the areas served by the affected nerves. Here, I’ll describe the anatomy related to common sites of nerve root compression at the C6, C7, L5, and S1 levels.

Cervical Spine (C6 and C7)
1. C6 Nerve Root:
Location: The C6 nerve root exits the spinal column between the C5 and C6 vertebrae.
Structure Implicated: Commonly compressed by herniated discs, degenerative changes, or osteophyte formation at the C5-C6 vertebral level.
Clinical Presentation: Compression here can cause pain and weakness in the biceps and wrist extensors, and numbness or tingling that radiates down the thumb side of the forearm and into the thumb.

  1. C7 Nerve Root:
    Location: The C7 nerve root exits between the C6 and C7 vertebrae.
    Structure Implicated: Like C6, it is prone to compression from herniated discs or osteophytes at the C6-C7 level.
    Clinical Presentation: Symptoms may include pain and weakness in the triceps and finger extensors, and numbness or tingling that extends down the middle finger.
    Lumbar Spine (L5 and S1)
  2. L5 Nerve Root:
    Location: The L5 nerve root exits the spinal column between the L4 and L5 vertebrae.
    Structure Implicated: Compression often occurs due to a herniated disc at the L4-L5 level, spondylolisthesis, or spinal stenosis.
    Clinical Presentation: Impingement can lead to pain and weakness in the dorsiflexors of the foot (lifting the foot upwards), and numbness along the top of the foot and into the big toe.
  3. S1 Nerve Root:
    Location: The S1 nerve root exits between the L5 and S1 vertebrae.
    Structure Implicated: Typically compressed by herniated discs at the L5-S1 level, spondylolisthesis, or spinal stenosis.
    Clinical Presentation: Symptoms include pain and weakness in the plantar flexors of the foot (pushing the foot downwards), and numbness or tingling that may radiate along the outer side of the foot and heel.

Common Compression Mechanisms:
Herniated Discs: Nucleus pulposus material can protrude through tears in the annulus fibrosus, pressing against nerve roots.
Osteophytes: Bone spurs from osteoarthritis can protrude into the spinal canal or foramina, compressing nerve roots.
Spondylolisthesis: One vertebra slipping over another can narrow the space through which the nerve root exits, causing compression.
Spinal Stenosis: Narrowing of the spinal canal or neural foramina can compress nerve roots; this is often due to a combination of disc degeneration, thickening of ligaments, and bone spur growth.

Diagnosis and Imaging:
MRI: Provides detailed images of soft tissues and bones, ideal for identifying disc herniations, ligament thickening, and osteophytes.
CT Scan: Useful for visualizing bone details and diagnosing osteophytes and spondylolisthesis.
X-rays: Can show alignment, vertebral slippage, and osteophytes but less detailed for soft tissue structures.

Understanding these anatomical details helps in diagnosing the specific levels of nerve root compression and planning appropriate treatment strategies, including physical therapy, medications, or potentially surgical interventions.

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2
Q

Joint structure of C spine

A
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3
Q

Cervical spine radiculopathy is more related to disc prolapse or bony disease?

A

Bony disease.
- Uncovertebral or facet joint arthritis.

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4
Q

Radicular radiation related to cervical radiculopathy may occur in what fraction of patients with cervical radiculopathy?

A

2/3

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5
Q

Other than pain, cervical radiculopathy commonly presents with what sign?

A

Depressed biceps and triceps reflexes.

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6
Q

What is the commonest cervical radiculopathy?

A

C7 radiculopathy (60%)
- The nerve root above the C7 vertebrae

Radiation is to the back of the forearm and into the middle fingers.
Depressed triceps reflex and muscle weakness.

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7
Q

What is the second commonest cervical radiculopathy?

A

C6 radiculopathy (20%)

Radiation to the superior lateral forearm and into the thumb and index fingers.

Weakness in the flexor carpi ulnaris (wrist flexion) but often uncertain.
Depressed biceps reflex.
Needs to be distinguished from CTS (carpal tunnel syndrome)

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8
Q

What is the more common cause of lumbar radiculopathy?
Disc herniation or spondylosis?

A

Disc herniation is far more common.

Very benign prognosis with 90% better within 3 months

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9
Q

What is the commonest lumbar radiculopathy?

A

It is the L5 radiculopathy.

This will usually present with paresthesia down the outer aspect of the leg and into the top of the foot.
Mild to moderate (but often symptomatic) weakness of dorsiflexion.

No reflex change
Need to differentiate it from a common peroneal nerve lesion.
- Can present with back pain, sensory change, and inversion as weak as eversion.

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10
Q

A patient with S1 radiculopathy would experience what symptoms?

A

Sensory changes running down the back of the leg and along the outside of the foot.

Weakness is rarely reported but commonly present. Unable to stand on tip toes on the affected foot.

Ankle jerk reflex suppressed

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11
Q

What levels are the ankle, patella, biceps, and triceps reflexes?

A
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12
Q

Disease of the atlanto-occipital joint can be associated with rheumatoid arthritis. This may lead to subluxation of C1 on C2 leading to what?

A

Paresthesia over the ear. Followed by medullary compression.

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13
Q

Is MRI or CT better for lumbar spine / C-spine

A

CT - Lumbar
MRI - C-spine

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14
Q

What are the three commonest focal mononeuropathies?

A

Carpal tunnel syndrome
Radial nerve palsy (saturday night palsy)
Common peroneal nerve palsy

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15
Q

How is carpal tunnel syndrome usually described?

A

Carpal tunnel syndrome (CTS) is commonly described as a condition that causes pain, numbness, and tingling in the hand and arm. The syndrome occurs when one of the major nerves to the hand—the median nerve—is compressed or squeezed as it travels through the wrist. Here’s a detailed breakdown of how carpal tunnel syndrome is typically described:

Anatomy Involved
Median Nerve: The primary nerve affected in CTS. This nerve provides sensation to the thumb, index, middle, and part of the ring fingers. It also controls some of the muscles at the base of the thumb.
Carpal Tunnel: A narrow passageway located on the palm side of the wrist, which houses the median nerve and tendons. It is bounded by bones and ligaments.

Symptoms
Numbness, Tingling, and Pain: Usually in the thumb, index, middle, and ring fingers. The sensation can be similar to the feeling of “pins and needles.”
Shock-like Sensations: These can radiate to the fingers.
Weakness: Patients may experience weakness in the hand and drop objects due to a lack of thumb muscle control.
Symptom Progression: Often symptoms start gradually and can be intermittent. As the condition worsens, symptoms may become constant and more severe.
Motor - weakness of abductor pollicus brevis, wasting, sparing of median long flexors.

Pathophysiology
Median Nerve Compression: The compression of the median nerve within the carpal tunnel is typically due to inflammation, swelling of the nerve itself, or increased pressure from surrounding tissues.

Risk Factors: Includes repetitive hand use, certain wrist positions, pregnancy, obesity, and conditions like diabetes, rheumatoid arthritis, and hypothyroidism.

Clinical Presentation
Nighttime Symptoms: Many patients report a worsening of symptoms during the night which may cause them to wake up.
Daytime Symptoms: Symptoms can be provoked or worsened by activities that involve prolonged wrist flexion or gripping.

Diagnosis
Clinical Examination: Includes Tinel’s sign (tapping over the median nerve at the wrist causes tingling in the fingers) and Phalen’s maneuver (holding the wrists in a flexed position leads to increased symptoms).
Electrophysiological Tests: Nerve conduction studies and electromyography can confirm median nerve compression and assess the severity.
Imaging: Ultrasound or MRI can be used to visualize the structure of the carpal tunnel and see any abnormalities.

Treatment
Conservative Management: Initial treatment often includes wrist splinting, especially at night, to alleviate symptoms by keeping the wrist in a neutral position. Nonsteroidal anti-inflammatory drugs (NSAIDs) may be used to reduce pain and inflammation.
Activity Modification: Changing patterns of hand use or ergonomic corrections can help alleviate symptoms.
Corticosteroid Injections: Can provide temporary relief by reducing inflammation and swelling within the carpal tunnel.
Surgery: Carpal tunnel release surgery is considered when conservative treatments fail. It involves cutting the ligament that forms the roof of the tunnel to relieve the pressure on the median nerve.

Carpal tunnel syndrome is a frequently encountered neuropathy, and its diagnosis is primarily clinical. Appropriate intervention can typically alleviate symptoms and prevent permanent nerve damage.

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16
Q

How is radial nerve palsy usually described?

A

Radial nerve palsy, often referred to as “Saturday night palsy,” is typically described as a neurological condition affecting the radial nerve, which impairs the affected individual’s ability to extend the wrist and fingers. This condition can arise from various causes, including compression, trauma, or injury to the radial nerve. Here’s a detailed breakdown of how radial nerve palsy is generally characterized:

Anatomy of the Radial Nerve
Path: The radial nerve is a major peripheral nerve of the arm that originates from the brachial plexus. It travels down the arm and supplies the muscles on the back of the arm and forearm, which are primarily responsible for extending the wrist and fingers.
Innervation: It provides motor innervation to the triceps brachii muscle of the upper arm, and to the extensor muscles of the forearm, which facilitate wrist and finger extension. It also provides sensory innervation to parts of the forearm and hand.

Symptoms of Radial Nerve Palsy
Motor Deficits:
Wrist Drop: The most characteristic symptom, where the patient is unable to extend the wrist at the joint, causing the wrist to hang limply.
Difficulty in Extending Fingers: Patients may not be able to straighten the fingers at the metacarpophalangeal joints.
Weakness in Arm: Difficulty in extending the elbow due to weakness in the triceps muscle, although this is less common.
Sensory Loss:
Numbness or Altered Sensation: This can occur on the back of the hand and on the outer surface of the forearm. Can also occur in the snuff box.
Patients often cant spread fingers as the ulnar intrinsic’s don’t work.

Causes
Compression: Prolonged pressure on the nerve, which can occur during sleep (hence “Saturday night palsy”), from wearing a tight cast, or from crutches. Often associated with sedated patients (alcohol, opiates)
Trauma: Fractures of the humerus bone or other injuries can directly damage the radial nerve.
Iatrogenic: Surgical procedures involving the arm may inadvertently affect the radial nerve.

Diagnosis
Clinical Examination: Physical examination revealing wrist drop and difficulty in finger extension are key indicators.
Nerve Conduction Studies and Electromyography (EMG): These tests help to confirm the diagnosis by assessing the electrical activity of muscles and the integrity of nerves.
Imaging: X-rays or MRI may be used to identify associated conditions such as fractures or to assess for other potential causes of nerve compression.

Treatment
Conservative Management:
Splinting: To support the wrist in an extended position, preventing further muscle shortening and joint stiffness.
Physical Therapy: To maintain muscle strength and joint range of motion.
Medication: Pain management with nonsteroidal anti-inflammatory drugs (NSAIDs) if required.
Surgical Intervention: In cases where nerve compression is due to mechanical causes (like tumors or fibrous bands) or trauma, surgical decompression or repair may be necessary.

Prognosis
The prognosis for radial nerve palsy depends on the underlying cause. If the nerve has been compressed without any anatomical disruption, recovery can be excellent with appropriate management. However, more severe injuries, such as those involving nerve transection or significant trauma, may require longer recovery times and potentially result in more permanent deficits.

Radial nerve palsy is generally well-managed with a combination of supportive care, physical therapy, and surgical intervention when necessary. Early diagnosis and treatment are crucial to maximize recovery and improve functional outcomes.

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17
Q

How is common peroneal nerve palsy usually described?

A

Common peroneal nerve palsy, also known as fibular nerve palsy, is a condition characterized by impairment of the peroneal nerve, which affects the ability to lift the foot at the ankle joint. This condition typically results in what is known as foot drop, where the foot drags during walking, and a characteristic high-stepping gait is adopted to compensate for the inability to lift the foot. Below is a detailed description of common peroneal nerve palsy:

Anatomy of the Common Peroneal Nerve
Path: The common peroneal nerve, a branch of the sciatic nerve, wraps from the back of the thigh around the head of the fibula near the knee. It then divides into superficial and deep branches.

Innervation:
The deep peroneal nerve innervates the anterior muscles of the lower leg, which are primarily responsible for dorsiflexion of the foot and toes (lifting the foot upward).
The superficial peroneal nerve innervates the lateral leg muscles that evert the foot (turning the sole of the foot outward).

Symptoms of Common Peroneal Nerve Palsy
Affects all the extensor compartment muscles of the leg. Look for weakness of the tibialis anterior (everts foot) and posterior (helps invert foot).
Motor Deficits:
Foot Drop: Most notably, the affected individual cannot dorsiflex the foot, causing the foot to drop and drag along the ground when walking.
Toe Drop: Difficulty in lifting the toes.
Gait Alteration: Development of a high-stepping gait to prevent the toes from catching on the ground.
Sensory Loss:
Numbness or altered sensation along the anterolateral aspect of the lower leg and the dorsum of the foot.

Causes
Compression: The nerve’s superficial location near the fibular head makes it susceptible to compression by external forces. Prolonged crossing of the legs, plaster casts, and tight boots are common culprits.
Trauma: Fractures, dislocations, or direct blows to the knee can damage the nerve.
Surgical Procedures: Procedures around the knee may inadvertently affect the peroneal nerve.
Systemic Conditions: Conditions like diabetes mellitus can predispose individuals to nerve compressions due to a general susceptibility to peripheral neuropathies.

Diagnosis
Clinical Examination: Observation of gait, assessment of muscle strength in foot and toe dorsiflexion, and testing for sensory deficits.
Nerve Conduction Studies and Electromyography (EMG): To evaluate the electrical activity of muscles and the integrity of the nerve along its course.
Imaging: MRI or ultrasound may be used to identify the site of nerve compression or to visualize any structural anomalies causing nerve damage.

Treatment
Conservative Management:
Physical Therapy: To strengthen the muscles and maintain range of motion.
Orthotic Devices: Ankle-foot orthoses (AFO) may be used to support the foot in a normal position, aiding in walking and preventing injuries.
Medication: Anti-inflammatory drugs for pain and inflammation.
Surgical Intervention: If the palsy is due to compression by a cyst or other growths, surgical decompression or removal might be necessary. Surgery may also be considered in chronic or severe cases where no improvement is seen with conservative measures.

Prognosis
Recovery from common peroneal nerve palsy depends on the severity of the nerve damage and the underlying cause. Mild cases, especially those caused by reversible compression, often recover fully with appropriate treatment. Severe injuries involving nerve transection or significant trauma may have a poorer prognosis and might not recover completely.

Common peroneal nerve palsy is a relatively common neurologic condition that can significantly impact mobility and quality of life. Timely and appropriate management is crucial to improving outcomes and helping patients regain functional use of their foot and ankle.

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18
Q

What are common causes of provoked seizures?

A

Alcohol and BDZ withdrawal.
Medications
Metabolic

The seizure must occur within the first week of insult (usually first few days).

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19
Q

Acute symptomatic seizures are caused by?

A

They are early seizures associated with acute CNS insult, stroke, meningitis, head trauma.

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20
Q

Unprovoked seizures are associated with?

A

Seizures with an epileptic syndrome.

Remote seizures - seizures associated with previous cerebral insult, stroke, head trauma

21
Q

What is the average likelihood of further seizures within the next two years following a first seizure?

A

It is 40%.
Neuroimaging and EEG can provide more info to help with prognostication.
- Epileptiform activity on EEG >60% chance of further seizures
- Focal lesion on MRI > 60% chance of further seizures.

Once you have had 2 unprovoked seizures the risk is >70% for ongoing seizures.

22
Q

What is the practical definition of epilepsy?

A

At least two unprovoked (or reflex) seizures occurring > 24 hours apart.

One unprovoked seizure and a probability of further seizures similar to the general recurrence risk (at least 60%) after two unprovoked seizures, occurring over the next 10 years.

23
Q

What is the lifetime risk of having at least one seizure for the average person?

A

Its 5-10%
About 1/3 will happen to children (febrile seizures)
About 1/3 will be single seizures
And 1/3 will lead on to epilepsy

24
Q

What two age categories have a peak in the incidence of seizures?

A

Below 15
Over 60 (mainly due to strokes)

25
Q

What is the difference between generalised seizures and partial (focal) seizures?

A

Seizures are broadly categorized based on how and where abnormal brain activity begins and whether awareness is affected during the event. The two main categories are generalized seizures and partial (or focal) seizures, each with distinct characteristics:

Generalized Seizures:
Generalized seizures affect both hemispheres (sides) of the brain simultaneously and are characterized by widespread electrical discharges that involve the entire brain.
This category includes several different types of seizures:

1) Tonic-Clonic Seizures (formerly known as grand mal seizures): These are the most recognized type, characterized by an initial muscle stiffening (tonic phase) followed by rhythmic jerking movements (clonic phase).

2) Absence Seizures (formerly known as petit mal seizures): These are typically brief and may involve subtle body movements such as eyelid fluttering. The person usually stares blankly and does not respond to the environment during the seizure.

3) Myoclonic Seizures: These involve sudden, brief jerks or twitches of muscles or muscle groups.

4) Atonic Seizures (also known as drop attacks): During these seizures, there is a sudden loss of muscle tone leading to collapse or falling down.

5) Tonic Seizures: These involve a sudden stiffness of muscles, particularly those in the back, arms, and legs.

6) Clonic Seizures: These are characterized by rhythmic, jerking muscle contractions, usually affecting the neck, face, and arms.

People experiencing generalized seizures often lose consciousness or have changes in their level of awareness during the seizure.

Partial (Focal) Seizures
Partial seizures, now more commonly referred to as focal seizures, originate in a specific part of the brain and are categorized based on the level of awareness they affect:

1) Focal Aware Seizures (formerly known as simple partial seizures): During these seizures, the individual remains conscious and aware. Symptoms can include involuntary jerking of a body part, changes in emotions, sensations, and feelings, or sensory distortions such as tingling, dizziness, and seeing flashing lights.

2) Focal Impaired Awareness Seizures (formerly known as complex partial seizures): These seizures involve a change or loss of consciousness or awareness. Individuals may appear dazed and confused; they may not be able to respond to questions or directions. Actions during the seizure may seem purposeful but are unconscious, such as fumbling with clothes or smacking lips.

3) Focal to Bilateral Tonic-Clonic Seizures: These start in one part of the brain as a focal seizure but then spread to both sides of the brain, becoming a generalized tonic-clonic seizure. This progression involves the initial symptoms of a focal seizure followed by the general symptoms of a tonic-clonic seizure.

Summary of Differences
Origin of Seizure Activity:
Generalized Seizures: Begin and involve both sides of the brain simultaneously.
Partial (Focal) Seizures: Start in one specific area of the brain.
Consciousness:
Generalized Seizures: Typically involve loss of consciousness.
Partial Seizures: May or may not involve impairment of consciousness, depending on the type.

Symptoms:
Generalized Seizures: Often involve full-body spasms, stiffening, or jerks.
Partial Seizures: Symptoms are generally related to the brain area where the seizure begins and can be isolated to specific body parts or experiences.

Understanding the type of seizure an individual experiences is crucial for effective treatment and management, including the choice of medication, lifestyle adjustments, and, in some cases, surgical options to control seizures.

26
Q

How do you distinguish between temporal and extra-temporal seizures clinically?

A

Distinguishing between temporal lobe seizures (a subtype of focal seizures originating in the temporal lobe) and extratemporal seizures (originating outside the temporal lobe) involves careful consideration of the clinical manifestations, including the aura, the nature of the seizure activity, and postictal symptoms. Here’s how these types of seizures can typically be differentiated based on clinical presentation:

Temporal Lobe Seizures:
Temporal lobe seizures, particularly those affecting the mesial temporal lobe, are the most common type of focal epilepsy. They have distinct clinical features due to the temporal lobe’s role in emotion, memory, and sensory processing:

Aura: Often precedes the seizure; may include déjà vu (a sensation that one has lived through the present situation before), jamais vu (a sense that the familiar is strange or new), fear, or euphoria.
Autonomic Symptoms: Changes like flushing, pallor, sweating, or piloerection.
Olfactory or Gustatory Hallucinations: Unusual smells or tastes that aren’t actually present.
Psychic Symptoms: Including disturbances in perception, hallucinations, or dissociative experiences.
Motor Symptoms: Automatisms such as lip-smacking, chewing, fidgeting with hands, or repetitive swallowing.
Altered Consciousness: Typically, consciousness is impaired; patients may appear confused or dazed.
Duration: These seizures generally last a short period, usually 1 to 2 minutes.
Postictal State: Often includes memory impairment, confusion, fatigue, and sometimes headache, lasting minutes to hours.

Extratemporal Seizures
Seizures originating outside the temporal lobe can arise from various brain regions, such as the frontal, parietal, or occipital lobes. Their clinical features often reflect the functions of the affected area:

Frontal Lobe Seizures:
Motor Symptoms: Prominent and may include head and eye deviation, asymmetric posturing, or bicycling movements.
Speech Disturbances: If the dominant frontal lobe is involved.
Brief Duration: Typically last less than 30 seconds and may occur in clusters.
Preservation of Consciousness: More common in frontal seizures due to the brief nature and rapid spread.
Nocturnal Predominance: Frequently occur during sleep.

Parietal Lobe Seizures:
Sensory Symptoms: Such as tingling or numbness, localized to a specific part of the body.
Somatosensory Illusions or Hallucinations: Such as feelings of body distortion.

Occipital Lobe Seizures:
Visual Symptoms: Including flashing lights, hallucinations of shapes or colours.
Rapid Eye Blinking and Eye Movement: Often noted.

Diagnostic Tests
Electroencephalogram (EEG): While clinical symptoms guide the initial suspicion, EEG is crucial in localizing the origin of seizure activity. Temporal lobe seizures may show temporal spikes, while extratemporal seizures will have interictal spikes corresponding to different lobes.
Imaging: MRI can be used to identify structural causes of seizures, such as tumors, vascular malformations, or cortical dysplasia in respective brain regions.
Neuropsychological Testing: Helps to evaluate the cognitive functions specific to various brain regions, which may be affected by recurrent seizures.

Conclusion
In clinical practice, distinguishing between temporal and extratemporal seizures involves a detailed patient history to understand the sequence and nature of symptoms, backed by EEG and brain imaging. Accurate localization of seizure origin is essential for effective management, including medication, surgical intervention, and other treatments tailored to the specific type of epilepsy.

27
Q

What is juvenile myoclonic epilepsy?

A

Juvenile Myoclonic Epilepsy (JME) is a common type of epilepsy that typically presents during adolescence. This disorder is characterized primarily by myoclonic jerks—sudden, involuntary muscle spasms that often occur shortly after waking up. JME is classified under the category of genetic generalized epilepsies, indicating a genetic predisposition to this condition, often with a family history of seizures.

Key Characteristics of Juvenile Myoclonic Epilepsy:
Age of Onset: JME typically begins between the ages of 12 and 18. However, the onset can sometimes extend into the early twenties.

Seizure Types:
Myoclonic Seizures: These are the hallmark of JME and involve quick, involuntary muscle jerks. The jerks are typically bilateral and symmetric. They most commonly affect the shoulders, arms, and upper body, though legs can also be involved.

Generalized Tonic-Clonic Seizures (GTCS): Approximately 80-90% of patients with JME may experience GTCS at some point during their illness. These seizures can be more dramatic, involving stiffening of the body (tonic phase) followed by rhythmic jerking (clonic phase).

Absence Seizures: About one-third of patients may also experience absence seizures, which are brief episodes of staring or subtle body movements with unresponsiveness.

Diurnal Pattern:
Seizures in JME frequently occur shortly after waking up, often triggered by sleep deprivation, stress, or alcohol consumption.

Electroencephalogram (EEG):
EEG findings typically show generalized spike-and-wave or polyspike-and-wave discharges. These patterns are more pronounced during or after waking up and can be triggered by hyperventilation and photic stimulation during the EEG recording. 4-6 Hz frequency.

Trigger Factors:
Common triggers include sleep deprivation, alcohol intake, stress, and flickering lights (such as from computers, televisions, or strobe lights).

Treatment:
Medication: The mainstay of treatment for JME is antiepileptic drugs (AEDs). Valproate is highly effective and often the first choice in treatment, though it is avoided in women of childbearing age due to teratogenic risks. Other options include levetiracetam, lamotrigine, and topiramate.
Lifestyle Adjustments: Patients are advised to maintain a regular sleep schedule, avoid excessive alcohol consumption, and manage stress to help reduce the frequency of seizures.

Prognosis:
JME is a lifelong condition, and most patients will require long-term treatment with antiepileptic medications. While seizure control is typically good with medication, myoclonic jerks may persist despite treatment, and lapses in medication adherence or exposure to trigger factors can easily precipitate seizures.

Juvenile Myoclonic Epilepsy requires a careful and comprehensive management strategy that includes appropriate diagnosis, effective medication, and lifestyle modifications to manage seizures and maintain quality of life.

28
Q

What anti epileptic drugs are best for focal seizures?
What ones for generalised absence seizures? What ones offer broad cover of focal and general?

A

Focal seizures, think carbamazepine, phenytoin.

Generalised absence - think ethosuximide and acetozolamide

For broad cover of focal and generalised seizures things like valproate, lamotrigine, and topiramate are good.

29
Q

Who should avoid using sodium valproate?

A

Women of child bearing age should not use it due to its potential teratogenic effects

30
Q

What is Kernig’s sign?

A

Pain when flexing the hip and extending the knee.

It is used to assess for possible meningism.

Note in meningism the brain itself is not involved, so their should be no seizures, or disturbance to consciousness. (Except in late stages due to CSF obstruction or parenchymal invasion).

31
Q

What are the main causes of meningitis?

Bacterial
Viral
Fungal

A

Bacterial:
Streptococcus pneumoniae, Neisseria meningitidis (Meningococcus), Haemophilus influenzae type B (HiB), group B streptococcus, Listeria monocytogenes.

Streptococcus pneumoniae , S. pyogenes (Group A Streptococcus ; GAS) and S. agalactiae (Group B Streptococcus ; GBS) are major aetiological agents of diseases in humans.

Mycobacterium tuberculosis

Viral:
HSV2 recurrent meningitis
Non-polio enteroviruses (most don’t cause meningitis)
- e.g enterovirus D68 (EV-D68), enterovirus A71 (EV-A71), and coxsackie virus A6 (CV-A6)

Fungal:
Cryptococcus

The most common cause of meningitis varies by age group and geographic location, but overall, bacterial infections are among the leading causes. Here’s a breakdown of the most common bacterial agents:

Bacterial Meningitis
Neonates (birth to 1 month): The most common causes include Group B Streptococcus, Escherichia coli, and Listeria monocytogenes.
Infants and Children (1 month to 10 years): Streptococcus pneumoniae and Neisseria meningitidis are the predominant pathogens.
Adolescents and Young Adults (11 to 24 years): Neisseria meningitidis and Streptococcus pneumoniae. Meningococcal meningitis is particularly noted for its potential to cause outbreaks in college dormitories or military barracks.
Older Adults (over 50 years): Streptococcus pneumoniae, Neisseria meningitidis, and Listeria monocytogenes, with Listeria being more common in individuals over 60 years, particularly those with weakened immune systems.

Viral Meningitis
It’s important to note that viral meningitis, although generally less severe than bacterial meningitis, is more common overall. Viral (aseptic) meningitis can be caused by a variety of viral agents, including:

Enteroviruses: These are the most common viral cause and typically responsible for milder cases of meningitis.
Herpes Simplex Virus: Particularly HSV-2 is associated with meningitis, especially in adults.
Fungal and Parasitic Meningitis
These are less common and tend to occur predominantly in individuals with compromised immune systems. Fungal meningitis can be caused by organisms like Cryptococcus, especially in patients with HIV/AIDS.

Preventive Measures
Vaccinations: Effective vaccines are available for some of the leading causes of bacterial meningitis, including vaccines for Haemophilus influenzae type b (Hib), Streptococcus pneumoniae (pneumococcal), and Neisseria meningitidis (meningococcal).
Given the variety of organisms that can cause meningitis, accurate diagnosis through methods such as lumbar puncture (spinal tap) and identification of the specific causative agent is crucial for effective treatment. Bacterial meningitis is a medical emergency requiring immediate antibiotic therapy, whereas viral meningitis may often resolve without specific antiviral treatment.

32
Q

What are non infectious causes of meningism?

A

Blood - e.g. from subarachnoid haemorrhage

Malignant cells

Autoimmune - sarcoidosis, lupus, Behcet’s (a type of vasculitis)

Chemical - post neurosurgery

33
Q

When distinguishing encephalitis from meningitis what clinical signs may you look for?

A

Meningism symptoms almost certainly present in encephalitis.
But altered mental state, seizures, focal neurology, coma are all more specific for encephalitis.

34
Q

In which group of patients may you not see fever during meningitis?

A

Neonates or immune compromised.

35
Q

What would you expect to see in the CSF of a patient with bacterial meningitis vs viral vs fungal?

A

Cerebrospinal fluid (CSF) analysis is a critical diagnostic tool in differentiating between bacterial, viral, and fungal meningitis. Each type of meningitis has characteristic findings in the CSF that help guide diagnosis and management. Here’s what is typically observed in the CSF analysis for each type:

Bacterial Meningitis
Appearance: Cloudy or turbid due to the presence of bacteria and increased white blood cells.
White Blood Cell Count (WBC): Elevated, typically >1000 cells/µL; predominantly neutrophils.
Protein: Elevated, often >100 mg/dL or >0.5g/L
Glucose: Decreased relative to serum glucose (CSF glucose is usually <40% of serum glucose).
Opening Pressure: Often elevated.
Culture: Positive in most cases, identifying the causative bacteria.

Viral Meningitis
Appearance: Usually clear.
White Blood Cell Count (WBC): Moderately elevated, typically 10-500 cells/µL; predominantly lymphocytes.
Protein: Slightly elevated (>0.5g/L) or normal.
Glucose: Normal or mildly decreased (generally remains >60% of serum glucose).
Opening Pressure: Normal or slightly elevated.
Culture: Sterile; no bacteria grow. Viral PCR (polymerase chain reaction) tests can identify specific viruses.

Fungal Meningitis
Appearance: May be clear or slightly cloudy.
White Blood Cell Count (WBC): Moderately elevated; typically shows lymphocytes or a mixed response.
Protein: Elevated.
Glucose: Decreased.
Opening Pressure: Often elevated.
Culture and Other Tests: Fungal cultures are less sensitive and take longer; antigen tests, antibody tests, or PCR for fungi can aid in diagnosis. Cryptococcal meningitis can be diagnosed with a cryptococcal antigen test.

Additional Notes
CSF Lactate: This can be useful especially in differentiating bacterial from viral meningitis. Elevated levels are more suggestive of bacterial meningitis.
Gram Stain: Useful in bacterial meningitis; can provide rapid preliminary identification of bacteria.
India Ink Stain: Used historically for detection of Cryptococcus species in cases of suspected fungal meningitis.
Xanthochromia: The presence of bilirubin in CSF, tested in the evaluation of subarachnoid haemorrhage, can occasionally be relevant if differential diagnosis includes a haemorrhagic process.

When analysing CSF results, it’s important to consider that there can be overlap between different types of meningitis, especially in early stages or partially treated cases. Clinical correlation with patient symptoms, history, and other laboratory findings is crucial for accurate diagnosis and appropriate treatment.

36
Q

What is the empirical management for meningitis?

A

Empirical Antibiotic Therapy
The choice of empirical antibiotics depends on the patient’s age, predisposing conditions, and the most likely causative organisms:

Neonates (age 0-1 month):
Antibiotics: Ampicillin plus either cefotaxime or gentamicin.
Target Organisms: Group B streptococcus, Escherichia coli, Listeria monocytogenes.

Infants and Children (age 1 month to 18 years):
Antibiotics: A third-generation cephalosporin (e.g., cefotaxime or ceftriaxone) plus vancomycin.
Target Organisms: Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae type b.

Adults (age >18 years):
Antibiotics: Ceftriaxone or cefotaxime plus vancomycin.
Target Organisms: Streptococcus pneumoniae, Neisseria meningitidis. For adults over 50 years and those who are immunocompromised, ampicillin may be added to cover Listeria monocytogenes.

Elderly or Immunocompromised Individuals:
Antibiotics: Ampicillin is added to the regimen above to cover for Listeria monocytogenes, alongside coverage for other common pathogens with ceftriaxone or cefotaxime and vancomycin.

Adjunctive Therapy
Dexamethasone: This corticosteroid may be used in certain cases to reduce the inflammatory response in the brain that can lead to neurologic complications. Its use should be initiated before or with the first dose of antibiotics in cases of suspected or proven Streptococcus pneumoniae and Haemophilus influenzae type b meningitis. The benefits of dexamethasone in meningitis caused by other organisms are less clear.

Target Organism Coverage
Listeria monocytogenes is a key concern in patients over the age of 50, as well as in immunocompromised individuals, because these groups are at higher risk for Listeria infections, which can cause meningitis. Both ampicillin and benzylpenicillin are effective against Listeria. However, ampicillin is generally preferred for Listeria because of its broad spectrum of activity that also includes coverage against enterococci and some strains of Escherichia coli, providing a broader coverage that might be beneficial in a population at risk for a wider range of infections.
Streptococcus pneumoniae and Neisseria meningitidis are also significant concerns in older adults. While benzylpenicillin can be very effective against these pathogens, the choice to use it would depend on local resistance patterns. If penicillin resistance is low among Streptococcus pneumoniae isolates, benzylpenicillin could be a very effective choice.

37
Q

What is the definitive treatment for Neisseria meningitidis and for Streptococcus pneumonia induced meningitis?

A

N. m = penicillin

S. p = Pencillin, Ceftriaxone, vancomycin

38
Q

Compare the presentation of anterior cerebral artery strokes, middle cerebral artery strokes, posterior cerebral artery strokes, vertebral artery strokes, basilar artery strokes, and small vessel infarcts (lacunes).

A

Anterior Cerebral Artery (ACA) Strokes
Location Affected: Supplies the medial portions of the frontal lobes and the superior medial parietal lobes.
Symptoms:
Contralateral weakness and sensory loss, predominantly in the lower extremity. Gait apraxia.
Cognitive and behavioural disturbances, including abulia (lack of initiative) or akinetic mutism.
Urinary incontinence.
Grasp reflex, frontal release signs.

Middle Cerebral Artery (MCA) Strokes
Location Affected: Supplies the lateral part of the cerebral cortex, including the primary motor and sensory areas of the face, throat, hand, and arm, and in the dominant hemisphere, the areas responsible for speech.
Symptoms:
Contralateral paralysis and sensory impairment of the face and upper extremities more than the legs. Contralateral hemiparesis (muscle weakness).
If the dominant hemisphere is affected, aphasia (language disturbance) is common. Gertsmann syndrome also possible if parietal affected on dominant side (agraphia, acalculia, right/left confusion, finger agnosia).
If the non-dominant hemisphere is affected, symptoms may include spatial neglect and anosognosia (unawareness or denial of illness).
Homonymous hemianopia (optic radiations)

Posterior Cerebral Artery (PCA) Strokes
Location Affected: Supplies the occipital lobe and the bottom part of the temporal lobe.
Symptoms:
Contralateral hemianopia with macular sparing (vision loss in half the visual field but with central vision spared - distal MCA supplies it).
Memory impairment (if the medial temporal lobe is involved).
Visual agnosia and prosopagnosia (difficulty recognizing objects and faces, respectively), depending on the affected hemisphere. Bilateral hemianopia with cortical blindness (due to damage to occipital cortex)
Proximal - Thalamic syndrome with hemi-anaesthesia plus dystonia.

Vertebral Artery Strokes
Location Affected: Supplies the posterior part of the cerebellum and part of the brainstem.
Symptoms:
Ataxia and coordination problems.
Dizziness or vertigo.
Nystagmus.
Nausea and vomiting.
Crossed symptoms, where one side of the face and the opposite side of the body are affected, such as ipsilateral facial numbness and contralateral limb numbness.
Lateral Medullary Syndrome (PICA)
– Ipsilateral (numb face, Horner’s, nystagmus
and vocal cord paresis)
– Contralateral (impaired pain and temperature)
– Midline (hiccough, dysphagia)

Basilar Artery Strokes
Location Affected: Supplies the pons and other parts of the brainstem, as well as the cerebellum.
Symptoms:
Severe brainstem symptoms such as bilateral motor deficits, decreased consciousness, and cranial nerve disturbances.
Locked-in syndrome, where patients are alert and awake but cannot move or communicate due to paralysis of nearly all voluntary muscles in the body except for the eyes.
* Top of the Basilar syndrome
– Embolus: quadriparesis plus blindness
* Basilar occlusion
– Progressive deficits leading to coma
* Penetrating artery syndromes
– Multiple: may be para-median or lateral
– Mainly in the elderly

Small Vessel Infarcts (Lacunar Strokes)
Strongly associated with hypertension.
Location Affected: Small, deep arteries supplying the deep structures of the brain (basal ganglia, thalamus).
Symptoms:
Depending on the specific region affected, symptoms can include pure motor stroke, pure sensory stroke, clumsy hand-dysarthria, and ataxic hemiparesis.
Often, these strokes may be relatively silent or present with only mild symptoms compared to large artery strokes.

Summary
The clinical manifestations of stroke vary considerably and are influenced by the specific brain artery involved. Recognizing these patterns can aid in localizing the lesion and guiding further management and imaging studies. Prompt diagnosis and treatment are crucial to optimize outcomes in stroke patients

39
Q

What is amaurosis fugax?

A
  • Amaurosis fugax (transient monocular
    blindness): Patients describe it as “fog,
    shadow, blur, curtain”
  • Usually brief, 1-5 minutes
  • Strongly associated with ipsilateral carotid
    atheroma
  • Fortification spectra make it unlikely
40
Q

What is the most common type of headache?

A

Tension type headache.

They tend to occur as the day progresses and they are related to stress.

They can present as a bifrontal or bi-occipital throbbing or constant pain with no other associated features.
They may be 30 mins to 7 days.

Chronic if they occur more than 15 days per month.

41
Q

What is the treatment for tension type headaches?

A

Paracetamol, NSAIDs if used early are effective.

Prophylactic treatment includes:
- Antidepressant e.g. amitriptyline
- Anticonvulsants e.g. Topiramate
- Acupuncture
Preventative measures

42
Q

How do migraines usually present?

A

Unilateral severe throbbing headache
With or without preceding aura
Nausea, vomiting, and photophobia
Ask about family history, relationship to OC and food/alcohol

Episodic if less than 15 per month
Chronic if 15 or more days per month

More common in females.

Migraines + OC or smoking increase the risk of strokes

43
Q

How are migraines treated?

A

Abortive treatments:
- Take these early +/- anti emetic
- Voltaren rapid
- Triptans: flushing, chest pain
- Ergot preparations: nausea, vomiting, brady/tachycardia, confusion
- CGRP antibodies

Prophylactic
- Propranolol: not for asthmatics or athletes
- Vitamin B2
- Anticonvulsants: Valproate and topamax
- Antidepressants
- Botox
Acupuncture

44
Q

What is the moa of triptans?

A

Triptans are 5HT1B and 5HT1D serotonin receptor agonists.
They reduce symptoms or abort attacks in 70-80% of patients within 30-90 minutes.

Contraindicated in cardiovascular disease, stroke, Raynaud’s and hypertension.

DO NOT USE WITH ERGOT OR MAOI

45
Q

What is the role of CGRP in the management of migraines?

A

CGRP is a highly potent vasodilator

It is involved in the dilatation of cerebral and dural blood vessels and plays a role in the release of inflammatory mediators from mast cells.

CGRP participates in transmission of nociceptive messages to the brain and its levels are increased in migraine attacks and other neurovascular headaches. Levels normalise if patients are responsive to triptans.

CGRP antagonists are as effective as triptans for migraine treatment but have fewer side effects.

46
Q

What is the drug of choice for patients with hemiplegic migraines and what drugs should be avoided?

A

Topiramate is a good drug for these patients.

Avoid triptans in this group.

Hemiplegic migraines may be due to calcium or sodium channelopathies and can present similar to strokes with unilateral weakness, sensory symptoms, and migraines.

47
Q

How do cluster headaches present?

A

Unilateral stabbing pains
Cluster of stabs
Tearing of eye or running nose
Lasts for weeks
1-3 attacks per day

Coital headache is similar

48
Q

What is the management for cluster headaches?

A

High flow oxygen, short course oral steroids.

Verapamil can be used prophylactically