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    <text># Implications of Neurological diseases to the oral health care provider

Dr Guru O  
Oral Medicine Specialist</text>
    <formatted_text>#### Presentation Overview

This presentation addresses the clinical implications and management strategies for patients presenting with neurological diseases within a dental and oral health care setting.

#### Presenter Information

- **Specialist:** Dr. Guru O
- **Department:** Oral Medicine</formatted_text>
  </page>
  <page number="2">
    <text># Topics to cover

- Epilepsy
- Multiple sclerosis
- Parkinsons disease
- Stroke/cerebrovascular accident</text>
    <formatted_text>The following neurological conditions and their implications for oral health care providers will be addressed:

- Epilepsy
- Multiple sclerosis
- Parkinson&amp;apos;s disease
- Stroke / cerebrovascular accident</formatted_text>
  </page>
  <page number="3">
    <text>Epilepsy</text>
    <formatted_text>Epilepsy is a chronic neurological disorder characterized by recurrent, unprovoked seizures.</formatted_text>
  </page>
  <page number="4">
    <text>```markdown
Epilepsy – definitions

- **Seizure** is a paroxysmal alteration of neurologic function caused by the excessive, hypersynchronous discharge of neurons in the brain.

- Various causes of seizures:
  - Epileptic seizures – abnormal neuronal firing
  - Non-epileptic seizures – e.g. psychogenic seizures, hypoglycemia, fever. Some are from reversible causes and are secondary in nature.

- **Epilepsy** is the condition of recurrent, unprovoked seizures.

  - Epilepsy syndrome is a group of clinical characteristics that consistently occur together

Stafstrom et al 2015
```</text>
    <formatted_text>#### Core Definitions

- **Seizure**: A paroxysmal alteration of neurologic function caused by the excessive, hypersynchronous discharge of neurons in the brain.
- **Epilepsy**: The condition of recurrent, unprovoked seizures.
- **Epilepsy Syndrome**: A group of clinical characteristics that consistently occur together.

#### Causes of Seizures

- **Epileptic seizures**: Resulting from abnormal neuronal firing.
- **Non-epileptic seizures**: Resulting from reversible or secondary causes, such as psychogenic seizures, hypoglycemia, or fever.</formatted_text>
  </page>
  <page number="5">
    <text>```markdown
Epilepsy – epidemiology

• Gender: slight male predilection
• Age: 75% begins in childhood
• Incidence: 61.4 new cases per 100 000 persons per year
• Prevalence: 1% of the population, 0.33% refractory epilepsy (i.e. epilepsy not controlled by &amp;gt;2 AEDs).

(Beghi 2020)
```</text>
    <formatted_text>#### Statistical Overview

- **Gender**: Slight male predilection.
- **Age**: 75% of cases begin in childhood.
- **Incidence**: 61.4 new cases per 100,000 persons per year.
- **Prevalence**:
  - 1% of the general population.
  - 0.33% suffer from refractory epilepsy (epilepsy not controlled by more than two anti-epileptic drugs [AEDs]).</formatted_text>
  </page>
  <page number="6">
    <text># Epilepsy – Diagnosis and classification

International league against epilepsy (ILAE):

- Categories of seizures:
  - Generalised
    - Originate from bilateral distributed neuronal networks
  - Focal (used to be called partial)
    - Originate from neuronal networks limited to part of one cerebral hemisphere
  - Spasms

Seizures can begin focally and later generalize

Seizures can originate in the cortex or subcortical structures

(Fisher et al 2017)</text>
    <formatted_text>#### ILAE Categories of Seizures

According to the International League Against Epilepsy (ILAE), seizures are categorized based on their origin:

- **Generalised**: Originate from bilateral distributed neuronal networks.
- **Focal (formerly Partial)**: Originate from neuronal networks limited to part of one cerebral hemisphere.
- **Spasms**.

#### Key Characteristics

- Seizures can begin focally and later generalize.
- Seizures can originate in the cerebral cortex or subcortical structures.</formatted_text>
  </page>
  <page number="7">
    <text># Epilepsy – Classification

International league against epilepsy (ILAE):
- Categories of seizures:
  - Generalised seizures
    - Further classified into:
      - Absence (petit mal)
        - Starting with unresponsiveness to external verbal stimuli, sometimes with eye blinking or head nodding
      - Generalised tonic-clonic (GTC) (grand mal)
        - Bilateral symmetric convulsive movements of all limbs with impairment of consciousness
      - Myoclonic
        - Sudden brief (lightning fast) movements that are not associated with any obvious disturbance of consciousness
        - These can be general or focal
      - Atonic
        - Involve the loss of body tone, often resulting in a head drop or fall
  - Focal seizures
    - Clinical manifestation depends on area of cortex involved
  - Epileptic Spasms
    - Sudden extension or flexion of extremities, held for several seconds, then reoccur in clusters.
    - (Fisher et al 2017)</text>
    <formatted_text>#### Detailed Seizure Classification

1. **Generalised Seizures**
  - **Absence (petit mal)**: Characterized by unresponsiveness to external verbal stimuli, sometimes accompanied by eye blinking or head nodding.
  - **Generalised tonic-clonic (GTC) (grand mal)**: Bilateral symmetric convulsive movements of all limbs with impairment of consciousness.
  - **Myoclonic**: Sudden, brief (lightning-fast) movements not associated with obvious disturbance of consciousness; can be general or focal.
  - **Atonic**: Involves the loss of body tone, often resulting in a head drop or fall.

2. **Focal Seizures**
  - Clinical manifestations depend on the specific area of the cortex involved.

3. **Epileptic Spasms**
  - Sudden extension or flexion of extremities, held for several seconds, typically occurring in clusters.</formatted_text>
  </page>
  <page number="8">
    <text># Epilepsy – Classification

## ILAE 2017 Classification of Seizure Types Expanded Version¹

| Focal Onset | Generalized Onset | Unknown Onset |
| --- | --- | --- |
| **Aware** | **Impaired Awareness** |  |
| **Motor Onset** | **Motor** | **Motor** |
| automatisms | tonic-clonic | tonic-clonic |
| atonic² | clonic | epileptic spasms |
| clonic | tonic |  |
| epileptic spasms² | myoclonic |  |
| hyperkinetic | myoclonic-tonic-clonic |  |
| myoclonic | myoclonic-atonic |  |
| tonic | atonic |  |
| **Nonmotor Onset** | **Nonmotor (absence)** | **Nonmotor** |
| autonomic | typical | behavior arrest |
| behavior arrest | atypical |  |
| cognitive | myoclonic |  |
| emotional | eyelid myoclonia |  |
| sensory |  |  |
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![](L25 Neurological diseases_figures/img_ff8a4dc89614aa82.webp)</text>
    <formatted_text>#### ILAE 2017 Classification of Seizure Types (Expanded)

| Focal Onset | Generalized Onset | Unknown Onset |
| :--- | :--- | :--- |
| **Aware / Impaired Awareness** | | |
| **Motor Onset** | **Motor** | **Motor** |
| - Automatisms | - Tonic-clonic | - Tonic-clonic |
| - Atonic | - Clonic | - Epileptic spasms |
| - Clonic | - Tonic | |
| - Epileptic spasms | - Myoclonic | |
| - Hyperkinetic | - Myoclonic-tonic-clonic | |
| - Myoclonic | - Myoclonic-atonic | |
| - Tonic | - Atonic | |
| **Nonmotor Onset** | **Nonmotor (absence)** | **Nonmotor** |
| - Autonomic | - Typical | - Behavior arrest |
| - Behavior arrest | - Atypical | |
| - Cognitive | - Myoclonic | |
| - Emotional | - Eyelid myoclonia | |
| - Sensory | | |</formatted_text>
    <images>
      <img bbox="257,270,689,847" type="diagram" path="L25 Neurological diseases_figures/img_ff8a4dc89614aa82.webp">
        <description>The image displays a diagram titled &amp;quot;ILAE 2017 Classification of Seizure Types Expanded Version,&amp;quot; which categorizes seizure types into three main groups: Focal Onset, Generalized Onset, and Unknown Onset. Each group is further divided into subtypes such as motor and nonmotor onset, with specific examples listed under each category. The diagram provides a structured classification system for different types of seizures, including tonic-clonic, absence, and myoclonic seizures, among others.</description>
      </img>
    </images>
  </page>
  <page number="9">
    <text># Epilepsy – Diagnosis

- History and examination
- EEG, preferably:
  - Wakefulness, drowsiness and sleep.
- Neuroimaging
  - Usually MRI
  - CT is useful in the acute setting – to detect hemorrhage, calcification or tumors.
- Metabolic evaluation
- Genetic testing

(Fisher et al 2017)</text>
    <formatted_text>#### Diagnostic Protocols

- **Clinical Assessment**: Comprehensive history and physical examination.
- **Electroencephalogram (EEG)**: Preferably capturing wakefulness, drowsiness, and sleep.
- **Neuroimaging**:
  - **MRI**: Standard imaging modality.
  - **CT**: Useful in acute settings to detect hemorrhage, calcification, or tumors.
- **Laboratory Testing**: Metabolic evaluation and genetic testing.</formatted_text>
  </page>
  <page number="10">
    <text># Epilepsy – comorbidities

- Psychiatric disorders:
  - Depression, anxiety, learning disability, ADHD, intellectual disability and autism
  - Previously considered secondary to uncontrolled seizure or medication, are now recognised as an integral part of the disorders, sometimes even preceding the seizures.

(Stafstrom et al 2015)</text>
    <formatted_text>#### Psychiatric and Developmental Comorbidities

- Common comorbidities include depression, anxiety, learning disabilities, ADHD, intellectual disability, and autism.
- These conditions are now recognized as integral parts of the seizure disorder rather than merely secondary effects of medication or uncontrolled seizures; they may even precede the onset of seizures.</formatted_text>
  </page>
  <page number="11">
    <text># Epilepsy – Dental chairside management

- Medical history – including the level of control of seizures
- Placement of ligated mouth prop at the beginning of procedure
- Supine position

If seizure occurs during the procedure:
- Clear the area
- Turn the patient to the side (to avoid aspiration)
- Passively restrain*

After the seizure:
- Examine traumatic injuries
- Discontinue treatment, arrange for patient transport
- If it’s a first seizure, patient should be evaluated in the emergency room.

(Little et al 2018)</text>
    <formatted_text>#### Pre-operative and Procedural Precautions

- Obtain a thorough medical history, specifically the level of seizure control.
- Place a ligated mouth prop at the beginning of the procedure.
- Utilize the supine position.

#### Management of Intra-operative Seizures

1. Clear the immediate area of hazards.
2. Turn the patient to their side to prevent aspiration.
3. Provide passive restraint (do not use force).

#### Post-seizure Protocol

- Examine the patient for traumatic injuries.
- Discontinue dental treatment and arrange for safe transport.
- If it is the patient&amp;apos;s first seizure, they must be evaluated in an emergency room.</formatted_text>
  </page>
  <page number="12">
    <text># Epilepsy – Dental chairside management

Most tonic-clonic seizures end in 1-2 minutes. There is also a post-ictal phase.

Status epilepticus occurs when:
- The active part of a tonic-clonic seizure lasts 5 minutes or longer
- A person goes into a second seizure without recovering consciousness from the first one
- If a person is having repeated seizures for 30 minutes or longer

(Wylie et al 2023)</text>
    <formatted_text>#### Seizure Duration and Status Epilepticus

Most tonic-clonic seizures resolve within 1–2 minutes, followed by a post-ictal phase.

**Status Epilepticus** is defined as an emergency occurring when:
- The active part of a tonic-clonic seizure lasts 5 minutes or longer.
- A person experiences a second seizure without recovering consciousness from the first.
- Repeated seizures occur for 30 minutes or longer.</formatted_text>
  </page>
  <page number="13">
    <text># Epilepsy – Dental chairside management

## Non-convulsive Status epilepticus
- Long or repeated absence or complex partial seizures
- The person may be confused or not fully aware of what is going on, but they are not ‘unconscious’, like in a tonic clonic seizure.
- These situations can be harder to recognize than convulsive seizures. Symptoms are more subtle and it’s hard to tell seizure symptoms from the recovery period.
- There is no consistent time-frame on when these seizures are called an emergency. It depends in part on how long a person’s typical seizures are and how often they occur.

(Wylie et al 2023)</text>
    <formatted_text>#### Non-convulsive Status Epilepticus

- Characterized by prolonged or repeated absence or complex partial seizures.
- The patient may appear confused or lack full awareness but is not &amp;quot;unconscious&amp;quot; in the traditional tonic-clonic sense.
- Recognition is difficult as symptoms are subtle and may mimic the recovery period.
- Emergency designation depends on the individual&amp;apos;s typical seizure patterns and frequency.</formatted_text>
  </page>
  <page number="14">
    <text>Multiple sclerosis</text>
    <formatted_text>Multiple Sclerosis (MS) is a chronic, inflammatory, demyelinating disease of the central nervous system.</formatted_text>
  </page>
  <page number="15">
    <text># Multiple sclerosis

- Definition: MS is an autoimmune disease of the CNS, which is characterized by inflammation, axonal injury, demyelination and gliosis and neuronal loss (Tafti et al 2024)

- Epidemiology (Dobson et al 2019):
  - Gender: 3:1 F:M ratio
  - Age: Onset typically 20-40 years of age, but can present at any age. Almost 10% of cases are present before the age of 18.
  - Race:
    - Higher in Europeans vs non-European populations (i.e. East Asian and African descent).
    - Interestingly has shown latitude based prevalence – i.e. higher in northern latitudes of Europe and the US.</text>
    <formatted_text>#### Definition

MS is an autoimmune disease of the Central Nervous System (CNS) characterized by inflammation, axonal injury, demyelination, gliosis, and neuronal loss.

#### Epidemiology

- **Gender**: 3:1 female-to-male ratio.
- **Age**: Onset typically occurs between 20–40 years; however, 10% of cases present before age 18.
- **Race and Geography**:
  - Higher prevalence in European populations compared to East Asian or African descent.
  - Latitude-based prevalence: Higher incidence in northern latitudes of Europe and the United States.</formatted_text>
  </page>
  <page number="16">
    <text>Multiple sclerosis

- Etiology:
  - Genetic susceptibility – HLA-DRB1*15
  - EBV
    - Symptomatic EBV infection increases the risk of getting MS
    - Mechanism: heterogenous, however the prevailing theory is molecular mimicry
  - Vitamin D deficiency (UVB)
  - Latitude based theory – however this trend appears to be decreasing.
  - Females (interestingly early 1900s M:F was 1:1. The increasing female trend has been attributed to smoking).

(Dobson et al 2019)</text>
    <formatted_text>#### Risk Factors and Etiology

- **Genetic Susceptibility**: Associated with HLA-DRB1*15.
- **Epstein-Barr Virus (EBV)**: Symptomatic infection increases MS risk, likely through molecular mimicry.
- **Environmental Factors**:
  - Vitamin D deficiency (related to UVB exposure).
  - Historical latitude trends (though these are currently decreasing).
- **Gender Trends**: The increasing female-to-male ratio since the early 1900s has been partially attributed to smoking habits.</formatted_text>
  </page>
  <page number="17">
    <text>Multiple sclerosis

• Pathogenesis:
• Pathologic hallmark of MS in perivenular inflammatory lesions, leading to demyelinating plaques.
• Common in: periventricular area, pons and spinal cord
• Inflammatory infiltrates contain:
• Predominantly CD8+ T lymphocytes
• B cell and plasma cells also present in much lower numbers
• Neurodegeneration involving microscopic damage to various components of the CNS, such as axons, neurons and synapses.

(Dobson et al 2019)</text>
    <formatted_text>#### Pathological Hallmarks

- **Demyelinating Plaques**: Perivenular inflammatory lesions found commonly in the periventricular area, pons, and spinal cord.
- **Inflammatory Infiltrates**: Predominantly composed of CD8+ T lymphocytes, with smaller numbers of B cells and plasma cells.
- **Neurodegeneration**: Microscopic damage to axons, neurons, and synapses throughout the CNS.</formatted_text>
  </page>
  <page number="18">
    <text>Multiple sclerosis

• Clinical features:

| Feature              | Percentage |
|----------------------|------------|
| Numbness, tingling  | 63.5%      |
| Cognitive dysfunction | 13.4%     |
| Depression          | 14.7%      |
| Fatigue             | 40.1%      |
| Muscle Spasms       | 17.2%      |
| Weakness            | 25.3%      |
| Walking difficulty  | 48.9%      |
| Vision problems     | 40.2%      |
| Dizziness           | 23.2%      |
| Pain                | 19.3%      |
| Bladder dysfunction | 11.1%     |
| Bowel dysfunction   | 5.7%       |

(USF Health 2024)

![](L25 Neurological diseases_figures/img_4b671b1e8fb930e0.webp)</text>
    <formatted_text>#### Clinical Features Prevalence

| Feature | Percentage |
| :--- | :--- |
| Numbness / Tingling | 63.5% |
| Walking difficulty | 48.9% |
| Vision problems | 40.2% |
| Fatigue | 40.1% |
| Weakness | 25.3% |
| Dizziness | 23.2% |
| Pain | 19.3% |
| Muscle Spasms | 17.2% |
| Depression | 14.7% |
| Cognitive dysfunction | 13.4% |
| Bladder dysfunction | 11.1% |
| Bowel dysfunction | 5.7% |</formatted_text>
    <images>
      <img bbox="383,242,872,776" type="diagram" path="L25 Neurological diseases_figures/img_4b671b1e8fb930e0.webp">
        <description>A diagram illustrating the clinical features of multiple sclerosis, with a central human silhouette surrounded by percentages and symptoms such as numbness (63.5%), fatigue (40.1%), and walking difficulty (48.9%). The diagram uses color-coded labels to highlight various symptoms and their prevalence.</description>
      </img>
    </images>
  </page>
  <page number="19">
    <text># Multiple sclerosis

- Classification:
  - Relapsing-remitting (RR):
    - 70-80% of MS
    - New or recurrent neurological symptoms that are consistent with MS
    - Symptoms lasting 24-48 hours
    - Symptoms developing over days to weeks
  - Primary progressive (PP):
    - 15-20% of MS
    - Gradual deterioration from onset without relapses
  - Secondary progressive (SP):
    - Following initial relapsing course, there is a more gradual neurological decline.
  - Progressive relapsing (PR)
    - 5% of MS cases.
    - Gradual deterioration with superimposed relapses
  - Fulminant:
    - Severe MS with multiple relapse and rapid progression
  - Benign:
    - Overall mild disability course with rare relapses
- Diagnosis: history, physical and MRI

(Tafti et al 2024)</text>
    <formatted_text>#### Disease Classifications

- **Relapsing-remitting (RR)**: (70-80% of cases) New or recurrent neurological symptoms lasting 24–48 hours, developing over days to weeks.
- **Primary progressive (PP)**: (15-20% of cases) Gradual deterioration from onset without distinct relapses.
- **Secondary progressive (SP)**: Gradual neurological decline following an initial relapsing course.
- **Progressive relapsing (PR)**: (5% of cases) Gradual deterioration with superimposed relapses.
- **Fulminant**: Severe course with multiple relapses and rapid progression.
- **Benign**: Mild disability with rare relapses.

#### Diagnosis

Diagnosis is based on clinical history, physical examination, and MRI findings.</formatted_text>
  </page>
  <page number="20">
    <text>Multiple sclerosis

• Management:
• Short term goals focus on decreasing MRI lesion activity
• Addressing possible underlying causes that could have triggered relapse (infection or metabolic derangement)
• Symptomatic management of neurologic symptoms
• Short course corticosteroids – particularly in an acute flare
• IV methylprednisolone 3-7 days course of 500 to 1000mg daily – followed by short taper
• Oral pred – 1250mg/day with or without short taper
• PLEX – every other day for a total of 3-7 treatments
• Long term goals: prevent secondary progressive MS
• Glatiramer acetate, interferon beta preparations, natalizumab, mitoxantrone, fingolimod
• Post treatment challenges: ensuring patient compliance and monitoring for drug toxicity

(Tafti et al 2024)</text>
    <formatted_text>#### Acute and Long-term Management

- **Short-term Goals**: Decrease MRI lesion activity and address triggers (infection/metabolic issues).
- **Acute Flare Management**:
  - IV Methylprednisolone: 500–1000mg daily for 3–7 days.
  - Oral Prednisone: 1250mg/day.
  - Plasmapheresis (PLEX): 3–7 treatments every other day.
- **Long-term Goals**: Prevent progression using Disease-Modifying Therapies (DMTs) such as Glatiramer acetate, interferon beta, natalizumab, mitoxantrone, and fingolimod.
- **Challenges**: Patient compliance and monitoring for drug toxicity.</formatted_text>
  </page>
  <page number="21">
    <text># Multiple sclerosis

- Prognosis:
  - Deterioration in functioning due to the disease, however patients do not die from the disease, rather the complications from it:
    - Infection (especially respiratory and urinary tract infections)
    - Conditions associated with advanced disability – aspiration pneumonia (due to dysphagia) and chronic respiratory disease in men
    - Sepsis
    - Skin disease

(Harding et al 2020)</text>
    <formatted_text>#### Prognosis and Complications

While MS causes significant functional deterioration, mortality is usually due to secondary complications rather than the disease itself:
- Infections (Respiratory and Urinary Tract).
- Aspiration pneumonia (due to dysphagia).
- Chronic respiratory disease.
- Sepsis.
- Skin disease.</formatted_text>
  </page>
  <page number="22">
    <text>Multiple sclerosis

• Dental management:
• Oral manifestations 2-3%:
• Facial pain:
• TN (5% of MS patients) – possible absence of trigger zones, with continuous pain with lower intensity.
• Trigeminal neuropathies – V2 and V3, burning, tingling, reduced sensation.
• Visual disturbance
• Dysarthria – slow, irregular speech with separation of syllables of words (‘scanning speech’).
• During an attack, patients may experience facial paresthesia, and muscles of facial expression can undulate in a wave like motion (myokymia). Has been described as a ‘bag of worms’ on palpation
• Muscle weakness

(Little et al 2018)</text>
    <formatted_text>#### Oral Manifestations (2-3% of patients)

- **Facial Pain**:
  - Trigeminal Neuralgia (TN): Occurs in 5% of MS patients; may lack trigger zones and present as continuous lower-intensity pain.
  - Trigeminal Neuropathies: Burning, tingling, or reduced sensation in V2 and V3 distributions.
- **Motor and Sensory Disturbances**:
  - Dysarthria: &amp;quot;Scanning speech&amp;quot; (slow, irregular speech with separated syllables).
  - Facial Myokymia: Wave-like muscle undulations (&amp;quot;bag of worms&amp;quot; sensation) during attacks.
  - Facial paresthesia and muscle weakness.
- **Visual disturbances**.</formatted_text>
  </page>
  <page number="23">
    <text>Multiple sclerosis

• Dental management:
  • Dental treatment:
    • Dental care to be completed during periods of remission
    • Monitoring for opportunistic infections (candidosis) after acute flares due to high dose corticosteroids
    • Xerostomia and medication induced hyposalivation
    • As fatigue is often reported in the afternoons, morning appts are preferable
    • Dental visits may need to be short depending on stage of disease
      • May require GA management in advanced stages

(Little et al 2018)</text>
    <formatted_text>#### Dental Treatment Considerations

- **Scheduling**: Perform elective care during periods of remission. Morning appointments are preferred due to afternoon fatigue.
- **Clinical Management**:
  - Monitor for opportunistic infections (e.g., Candidosis) following high-dose corticosteroid use.
  - Manage xerostomia and medication-induced hyposalivation.
  - Keep appointments short; advanced stages may require General Anesthesia (GA).</formatted_text>
  </page>
  <page number="24">
    <text>Parkinsons Disease</text>
    <formatted_text>Parkinson&amp;apos;s Disease (PD) is a progressive neurodegenerative movement disorder.</formatted_text>
  </page>
  <page number="25">
    <text># Parkinsons Disease

- Description:
  - Parkinsons disease is a progressive movement disorder of the nervous system (Armstrong et al 2020)

- Epidemiology (Bloem et al 2021):
  - Gender: M &amp;gt; F
  - Age: increasing incidence and prevalence with age.
    - However, 5-10 % &amp;lt; 50 and 25% &amp;lt; 65 years of age
    - Global burden has doubled in the last 2 decades
  - Incidence: 1100 Australians under 65 per year (young onset)
  - Prevalence: 150 000 patients with PD in Aus
    - 2nd most common neurological disease after dementia</text>
    <formatted_text>#### Epidemiology

- **Gender**: More common in males.
- **Age**: Incidence increases with age, though 25% of patients are under 65 (Young Onset).
- **Prevalence**:
  - 150,000 patients in Australia.
  - Second most common neurological disease after dementia.
  - Global burden has doubled in the last 20 years.</formatted_text>
  </page>
  <page number="26">
    <text># Parkinsons Disease

- Etiology:
  - Genetics
    - SNCA, LRRK2, PRKN, PINK1 and GBA
    - Important for treatment*
  - Environment
    - Pesticides
    - Head injury and TBI
    - Possible COVID-19?
  - Negative associations:
    - Smoking – mechanism: high dopamine levels assoc with smokers
    - Coffee drinking
    - Anti-inflammatory drug use
    - High plasma urate levels
    - Physical activity

(Bloem et al 2021)</text>
    <formatted_text>#### Etiological Factors

- **Genetic Factors**: Mutations in SNCA, LRRK2, PRKN, PINK1, and GBA.
- **Environmental Risks**: Pesticide exposure, head injuries, and Traumatic Brain Injury (TBI). Possible links to COVID-19 are being explored.
- **Negative Associations (Protective Factors)**:
  - Smoking (linked to high dopamine levels).
  - Coffee consumption.
  - Use of anti-inflammatory drugs.
  - High plasma urate levels.
  - Physical activity.</formatted_text>
  </page>
  <page number="27">
    <text># Parkinsons Disease

- Pathogenesis:
  - Complex interaction of:
    - Alpha synuclein aggregation
    - Dysfunction of mitochondria
    - Dysfunction of lysosomes or vesicle transport
    - Synaptic transport issues
    - Neuroinflammation
  - Resulting in:
    - Accelerated death of dopaminergic neurons
    - But involves multiple other motor and non-motor circuits.
    
(Bloem et al 2021)</text>
    <formatted_text>#### Pathogenesis

The disease involves a complex interaction resulting in the accelerated death of dopaminergic neurons and disruption of motor/non-motor circuits, driven by:
- Alpha-synuclein aggregation.
- Mitochondrial and lysosomal dysfunction.
- Vesicle and synaptic transport issues.
- Neuroinflammation.</formatted_text>
  </page>
  <page number="28">
    <text># Parkinsons Disease

• Management and prognosis:

| Phase                 | Questions                                                                 |
|----------------------|---------------------------------------------------------------------------|
| Prodromal period     | • When does Parkinson&amp;apos;s disease start?&amp;lt;br&amp;gt;• Will I become symptomatic?&amp;lt;br&amp;gt;• What can I do to prevent that from happening? |
| Diagnosis            | • What does Parkinson&amp;apos;s disease look like?&amp;lt;br&amp;gt;• What causes my Parkinson&amp;apos;s disease?&amp;lt;br&amp;gt;• Are my family members at increased risk too?&amp;lt;br&amp;gt;• Why me?&amp;lt;br&amp;gt;• What is my prognosis? |
| Initiate treatment   | • When should I start drug treatment?&amp;lt;br&amp;gt;• What drug is the best choice for me?&amp;lt;br&amp;gt;• Apart from the drugs, are there any other treatment options? |
| Response fluctuations | • Are these response fluctuations treatable?&amp;lt;br&amp;gt;• Are there any other treatment options? |
| Terminal phase       | • How will I die?&amp;lt;br&amp;gt;• Can anything be done in this late phase of Parkinson&amp;apos;s disease? |

Examples of the various questions that people with Parkinson&amp;apos;s disease might have during the consecutive phases of the disease

(Bloem et al 2021)

![](L25 Neurological diseases_figures/img_0caf6435cbc66c97.webp)</text>
    <formatted_text>#### Clinical Phases and Patient Concerns

- **Prodromal Period**: Focus on prevention and symptom onset.
- **Diagnosis**: Focus on cause, prognosis, and familial risk.
- **Initiate Treatment**: Selection of drug therapies and non-pharmacological options.
- **Response Fluctuations**: Management of treatment-related motor fluctuations.
- **Terminal Phase**: End-of-life care and late-stage management.</formatted_text>
    <images>
      <img bbox="134,406,873,773" type="diagram" path="L25 Neurological diseases_figures/img_0caf6435cbc66c97.webp">
        <description>A diagram illustrating the progression of Parkinson&amp;apos;s disease through various phases: prodromal period, diagnosis, initiate treatment, response fluctuations, and terminal phase. Each phase is represented by a loop in a red line, with corresponding questions that patients might have during each stage, such as &amp;apos;When does Parkinson&amp;apos;s disease start?&amp;apos; and &amp;apos;How will I die?&amp;apos;. The diagram visually represents the journey of the disease and the evolving concerns of patients.</description>
      </img>
    </images>
  </page>
  <page number="29">
    <text># Parkinsons Disease

- Oral manifestations:
  - Some evidence of increased risk of **caries and periodontal disease**:
    - Possible factors: motor impairment, apathy, depression and dementia
    - As the disease progresses, reliant on caregiver
- Mastication disorders:
  - Mastication and facial movements can be impaired in moderate-advanced PD and increase with progression.
- Bruxism:
  - Higher prevalence rhythmic masticatory muscle activity in REM and nREM sleep in PD compared to controls (Abe et al 2013)

(Zlotnik et al 2015)</text>
    <formatted_text>#### Hard Tissue and Muscular Issues

- **Caries and Periodontal Disease**: Increased risk due to motor impairment, apathy, depression, and dementia affecting oral hygiene.
- **Mastication Disorders**: Impaired chewing and facial movements in moderate-to-advanced stages.
- **Bruxism**: Higher prevalence of rhythmic masticatory muscle activity during both REM and nREM sleep.</formatted_text>
  </page>
  <page number="30">
    <text># Parkinsons Disease

- Oral manifestations:
  - Sialorrhea and drooling
    - Excessive saliva production OR decreased clearance of saliva
      - More likely the later related to dysphagia
    - Angular cheilitis due to changed environment

(Zlotnik et al 2015)</text>
    <formatted_text>#### Salivary Issues

- **Sialorrhea and Drooling**: Primarily caused by decreased clearance of saliva (dysphagia) rather than overproduction.
- **Angular Cheilitis**: Often secondary to chronic drooling.</formatted_text>
  </page>
  <page number="31">
    <text># Parkinsons Disease

- Oral manifestations:
  - Xerostomia:
    - Drug induced
      - TCAs, other antidepressants, antipsychotics, anticholinergics, beta blockers and antihistamines.
      - Patients suffering from urinary disorders which require xerogenci drugs
  - Taste disturbances:
    - Some reports indicating higher frequency of taste disturbance in this group of patients
    - Tends to increase with disease progress
    - Possible causes:
      - CNS degeneration
      - Depression, reduced salivary secretion, poor HI, GI diseases (causing Zn deficiency), medications and smoking.

(Zlotnik et al 2015)</text>
    <formatted_text>#### Sensory and Secretory Disturbances

- **Xerostomia**: Primarily drug-induced (TCAs, antipsychotics, anticholinergics, beta-blockers).
- **Taste Disturbances**: Frequency increases with disease progression. Potential causes include CNS degeneration, poor oral hygiene, zinc deficiency, and medications.</formatted_text>
  </page>
  <page number="32">
    <text># Parkinsons Disease

- Oral manifestations:
  - BMS
    - Lots of paper and literature suggest higher prevalence of BMS in PD patients – brought on by Clifford 1998 showing 24% prevalence in PD patients.
    - However more recent data of BMS in PD patients shows prevalence is 1.9%-5.1%.
      - All BMS in PD patients have been through postal surveys or questionnaires
    - Prevalence of BMS in clinical based epidemiological studies is: 1%-5.4%.
      - Little difference
    - Moreover, it is likely diagnosis of BMS in PD patients would decrease after clinical examination. Xerosomtia, loose fitting dentures etc are frequently reported in this population.
    - Case report of BMS being triggered after prescription of levodopa
      - One of the cross-sectional studies looking at BMS in PD patients found increasing prevalence of BMS on higher average levodopa equivalent dose.
    - Korean incidence study which compared BMS development in PD patient’s vs controls found no difference
      - (O et al 2023)</text>
    <formatted_text>#### Burning Mouth Syndrome (BMS)

- Reported prevalence varies significantly (1.9% to 24%).
- Clinical studies suggest the prevalence is actually low (1%–5.4%), similar to the general population.
- Many cases may be misdiagnosed xerostomia or ill-fitting dentures.
- There is a possible link between BMS symptoms and high-dose Levodopa therapy.</formatted_text>
  </page>
  <page number="33">
    <text># Parkinsons Disease

- Dental management:
  - Ensure rigorous hygiene plan for patient, involving the patient and caregivers. Recalls should be tailored to the individual.
  - COMT inhibitors – used to prolong the effect of levodopa
    - Tolcapone, entacapone
    - Can potentially interact with adrenaline in LA, however no reports of this.
    - However, be mindful not to go beyond to carpules containing 1:100 000 epinephrine (36micrograms)
    - Orthostatic hypotension is common in PD patients + side effect of COMT inhibitors
      - Chair should be inclined slowly for patients at the end of the appt
  - Pramipexole (dopamine agonist) interacts with erythromycin
  - Timing of appointment: during time of day at which their medication has maximum effect. Need to check this with patient. Usually, 1-3 hours after consuming medication.

(Little et al 2018)</text>
    <formatted_text>#### Clinical Management

- **Hygiene**: Rigorous plans involving caregivers; tailored recall intervals.
- **Pharmacological Interactions**:
  - **COMT Inhibitors (e.g., Entacapone)**: Limit epinephrine in local anesthesia to two cartridges (36 micrograms).
  - **Dopamine Agonists (e.g., Pramipexole)**: Interacts with erythromycin.
- **Safety**: Monitor for orthostatic hypotension; incline the dental chair slowly.
- **Scheduling**: Time appointments 1–3 hours after medication intake for maximum effect.</formatted_text>
  </page>
  <page number="34">
    <text>Stroke/Cerebrovascular accident</text>
    <formatted_text>Stroke, or Cerebrovascular Accident (CVA), is a critical condition resulting from disrupted blood flow to the brain.</formatted_text>
  </page>
  <page number="35">
    <text># Stroke/Cerebrovascular accident

**Definition:** sudden interruption of oxygenated blood to the brain.
- Subsequently, there is ischemic injury which leads to focal necrosis.

**Risk factors:**
- Hypertension, congestive heart failure, diabetes mellitus, previous CVA or transient ischemic attacks, &amp;gt;75 years, hypercholesterolemia, coronary atherosclerosis, smoking

(Little et al 2018)</text>
    <formatted_text>#### Definition

A sudden interruption of oxygenated blood to the brain, leading to ischemic injury and focal necrosis.

#### Risk Factors

- Hypertension and Congestive Heart Failure.
- Diabetes Mellitus.
- Previous CVA or Transient Ischemic Attacks (TIAs).
- Age &amp;gt; 75 years.
- Hypercholesterolemia and Coronary Atherosclerosis.
- Smoking.</formatted_text>
  </page>
  <page number="36">
    <text># Stroke/Cerebrovascular accident

## Complications:
- Death
  - Ischemic stroke: 8%
  - Hemorrhagic stroke: 38-47%
  - Overall, 23% die within the 1st year.
- Survive:
  - 10% will recover with no impairment
  - 50% will have mild residual disability
  - 15-30% are disabled will require special services
  - 10-20% require institutionalization

(Little et al 2018)</text>
    <formatted_text>#### Mortality and Disability Outcomes

- **Mortality Rates**:
  - Ischemic stroke: 8%
  - Hemorrhagic stroke: 38–47%
  - Overall: 23% die within the first year.
- **Recovery Statistics**:
  - 10% full recovery.
  - 50% mild residual disability.
  - 15–30% severe disability.
  - 10–20% require institutional care.</formatted_text>
  </page>
  <page number="37">
    <text>```markdown
Stroke/Cerebrovascular accident

Oral manifestations:
- Slurred speech
- Weak muscles
- Difficulty swallowing
- Unilateral paralysis of the facial musculature
- Loss of sensation
- Difficulty maintaining oral hygiene due to motor impairment

(Little et al 2018)
```</text>
    <formatted_text>#### Oral and Neurological Manifestations

- Slurred speech and difficulty swallowing.
- Unilateral facial paralysis and loss of sensation.
- Weakened musculature.
- Impaired ability to maintain oral hygiene due to motor deficits.</formatted_text>
  </page>
  <page number="38">
    <text># Stroke/Cerebrovascular accident

## Dental implications:
- Defer elective treatment until patient is stable
- Physical disability:
  - Assistance in oral hygiene measures
  - Chairside assistance to maneuver
- Good anxiety control, short, stress-free appointment
- Patient likely on antiplatelet and or anti-coagulant therapy as a preventative
  - Medication interactions e.g. with warfarin

(Little et al 2018)</text>
    <formatted_text>#### Dental Treatment Modifications

- **Stability**: Defer elective treatment until the patient is medically stable.
- **Appointment Management**: Short, stress-free appointments with good anxiety control.
- **Physical Assistance**: Help with maneuvering in the chair and modified oral hygiene instructions.
- **Pharmacology**: Be aware of antiplatelet or anticoagulant therapy (e.g., Warfarin) and potential drug interactions.</formatted_text>
  </page>
  <page number="39">
    <text># Stroke/Cerebrovascular accident

Communication tips:
- Face the patient
- Use slower, more deliberate speech
- Use drawings to explain procedures
- Get immediate feedback
- Do not underestimate or overestimate abilities
- Do not wear a mask when talking to the patient
- Communicate with personal carer

(Little et al 2018)</text>
    <formatted_text>#### Communication Strategies

- Face the patient directly and do not wear a mask while speaking.
- Use slow, deliberate speech and drawings for explanations.
- Seek immediate feedback to ensure understanding.
- Communicate with personal caregivers.
- Avoid underestimating or overestimating the patient&amp;apos;s cognitive or physical abilities.</formatted_text>
  </page>
  <page number="40">
    <text>Thank you – references

• Abe S., Gagnon J.-F., Montplaisir J. Y., Postuma R. B., Rompré P. H., Huynh N. T., Kato T., Kawano F., and Lavigne G. J., Sleep bruxism and oromandibular myoclonus in rapid eye movement sleep behavior disorder: a preliminary report, Sleep Medicine. (2013) 14, no. 10, 1024–1030, 2-s2.0-84883826735,
• Armstrong MJ, Okun MS. Diagnosis and Treatment of Parkinson Disease: A Review. JAMA. 2020 Feb 11;323(6):548-560. doi: 10.1001/jama.2019.22360. PMID: 32044947.
• Beghi E. The Epidemiology of Epilepsy. Neuroepidemiology. 2020;54(2):185-191. doi: 10.1159/000503831. Epub 2019 Dec 18. PMID: 31852003.
• Bloem BR, Okun MS, Klein C. Parkinson&amp;apos;s disease. Lancet. 2021 Jun 12;397(10291):2284-2303. doi: 10.1016/S0140-6736(21)00218-X. Epub 2021 Apr 10. PMID: 33848468.
• Dobson R, Giovannoni G. Multiple sclerosis - a review. Eur J Neurol. 2019 Jan;26(1):27-40. doi: 10.1111/ene.13819. Epub 2018 Nov 18. PMID: 30300457
• Fisher RS, Cross JH, French JA, Higurashi N, Hirsch E, Jansen FE, Lagae L, Moshé SL, Peltola J, Roulet Perez E, Scheffer IE, Zuberi SM. Operational classification of seizure types by the International League Against Epilepsy: Position Paper of the ILAE Commission for Classification and Terminology. Epilepsia. 2017 Apr;58(4):522-530. doi: 10.1111/epi.13670. Epub 2017 Mar 8. PMID: 28276060.
• Harding K, Zhu F, Alotaibi M, Duggan T, Tremlett H, Kingwell E. Multiple cause of death analysis in multiple sclerosis: A population-based study. Neurology. 2020 Feb 25;94(8):e820-e829. doi: 10.1212/WNL.0000000000008907. Epub 2020 Jan 13. PMID: 31932517; PMCID: PMC7136054.
• Kalf JG, Bloem BR, Munneke M. Diurnal and nocturnal drooling in Parkinson&amp;apos;s disease. J Neurol. 2012 Jan;259(1):119-23. doi: 10.1007/s00415-011-6138-2. Epub 2011 Jun 23. PMID: 21698387; PMCID: PMC3251785.</text>
    <formatted_text>- Abe S., Gagnon J.-F., Montplaisir J. Y., Postuma R. B., Rompré P. H., Huynh N. T., Kato T., Kawano F., and Lavigne G. J., Sleep bruxism and oromandibular myoclonus in rapid eye movement sleep behavior disorder: a preliminary report, Sleep Medicine. (2013) 14, no. 10, 1024–1030, 2-s2.0-84883826735.
- Armstrong MJ, Okun MS. Diagnosis and Treatment of Parkinson Disease: A Review. JAMA. 2020 Feb 11;323(6):548-560. doi: 10.1001/jama.2019.22360. PMID: 32044947.
- Beghi E. The Epidemiology of Epilepsy. Neuroepidemiology. 2020;54(2):185-191. doi: 10.1159/000503831. Epub 2019 Dec 18. PMID: 31852003.
- Bloem BR, Okun MS, Klein C. Parkinson&amp;apos;s disease. Lancet. 2021 Jun 12;397(10291):2284-2303. doi: 10.1016/S0140-6736(21)00218-X. Epub 2021 Apr 10. PMID: 33848468.
- Dobson R, Giovannoni G. Multiple sclerosis - a review. Eur J Neurol. 2019 Jan;26(1):27-40. doi: 10.1111/ene.13819. Epub 2018 Nov 18. PMID: 30300457.
- Fisher RS, Cross JH, French JA, Higurashi N, Hirsch E, Jansen FE, Lagae L, Moshé SL, Peltola J, Roulet Perez E, Scheffer IE, Zuberi SM. Operational classification of seizure types by the International League Against Epilepsy: Position Paper of the ILAE Commission for Classification and Terminology. Epilepsia. 2017 Apr;58(4):522-530. doi: 10.1111/epi.13670. Epub 2017 Mar 8. PMID: 28276060.
- Harding K, Zhu F, Alotaibi M, Duggan T, Tremlett H, Kingwell E. Multiple cause of death analysis in multiple sclerosis: A population-based study. Neurology. 2020 Feb 25;94(8):e820-e829. doi: 10.1212/WNL.0000000000008907. Epub 2020 Jan 13. PMID: 31932517; PMCID: PMC7136054.
- Kalf JG, Bloem BR, Munneke M. Diurnal and nocturnal drooling in Parkinson&amp;apos;s disease. J Neurol. 2012 Jan;259(1):119-23. doi: 10.1007/s00415-011-6138-2. Epub 2011 Jun 23. PMID: 21698387; PMCID: PMC3251785.</formatted_text>
  </page>
  <page number="41">
    <text>Thank you – references continued....

• Little J, Miller C, Rhodus N. Little and Falace&amp;apos;s Dental Management of the Medically Compromised Patient. 9 ed: Elsevier Health Sciences; 2018.
• O G, Balasubramaniam R, Klasser GD. Burning mouth disorder and Parkinson&amp;apos;s disease: A scoping review of the literature. J Oral Rehabil. 2023 Jun;50(6):488-500. doi: 10.1111/joor.13443. Epub 2023 Mar 22. PMID: 36855821.
• Parkinsons UK, 2024, ‘Mouth and dental issues’, accessed 19.09.2024, URL: https://www.parkinsons.org.uk/information-and-support/mouth-and-dental-issues
• Rana AQ, Yousuf MS, Awan N, Fattah A. Impact of progression of Parkinson&amp;apos;s disease on drooling in various ethnic groups. Eur Neurol. 2012;67(5):312-4. doi: 10.1159/000336054. Epub 2012 Apr 20. PMID: 22517489.
• Stafstrom CE, Carmant L. Seizures and epilepsy: an overview for neuroscientists. Cold Spring Harb Perspect Med. 2015 Jun 1;5(6):a022426. doi: 10.1101/cshperspect.a022426. PMID: 26033084; PMCID: PMC4448698.
• Tafti D, Ehsan M, Xixis KL. Multiple Sclerosis. [Updated 2024 Mar 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499849/
• USF Health (2024), ‘Symptoms of MS’, accessed 19.09.2024, ULR: https://health.usf.edu/medicine/neurology/multiple-sclerosis/symptoms-ms
• Wylie T, Sandhu DS, Murr NI. Status Epilepticus. [Updated 2023 May 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430686/
• Zlotnik Y, Balash Y, Korczyn AD, Giladi N, Gurevich T. Disorders of the oral cavity in Parkinson&amp;apos;s disease and parkinsonian syndromes. Parkinsons Dis. 2015;2015:379482. doi: 10.1155/2015/379482. Epub 2015 Jan 15. PMID: 25685594; PMCID: PMC4312641.</text>
    <formatted_text>- Little J, Miller C, Rhodus N. Little and Falace&amp;apos;s Dental Management of the Medically Compromised Patient. 9 ed: Elsevier Health Sciences; 2018.
- O G, Balasubramaniam R, Klasser GD. Burning mouth disorder and Parkinson&amp;apos;s disease: A scoping review of the literature. J Oral Rehabil. 2023 Jun;50(6):488-500. doi: 10.1111/joor.13443. Epub 2023 Mar 22. PMID: 36855821.
- Parkinsons UK, 2024, ‘Mouth and dental issues’, accessed 19.09.2024, URL: https://www.parkinsons.org.uk/information-and-support/mouth-and-dental-issues
- Rana AQ, Yousuf MS, Awan N, Fattah A. Impact of progression of Parkinson&amp;apos;s disease on drooling in various ethnic groups. Eur Neurol. 2012;67(5):312-4. doi: 10.1159/000336054. Epub 2012 Apr 20. PMID: 22517489.
- Stafstrom CE, Carmant L. Seizures and epilepsy: an overview for neuroscientists. Cold Spring Harb Perspect Med. 2015 Jun 1;5(6):a022426. doi: 10.1101/cshperspect.a022426. PMID: 26033084; PMCID: PMC4448698.
- Tafti D, Ehsan M, Xixis KL. Multiple Sclerosis. [Updated 2024 Mar 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499849/
- USF Health (2024), ‘Symptoms of MS’, accessed 19.09.2024, URL: https://health.usf.edu/medicine/neurology/multiple-sclerosis/symptoms-ms
- Wylie T, Sandhu DS, Murr NI. Status Epilepticus. [Updated 2023 May 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430686/
- Zlotnik Y, Balash Y, Korczyn AD, Giladi N, Gurevich T. Disorders of the oral cavity in Parkinson&amp;apos;s disease and parkinsonian syndromes. Parkinsons Dis. 2015;2015:379482. doi: 10.1155/2015/379482. Epub 2015 Jan 15. PMID: 25685594; PMCID: PMC4312641.</formatted_text>
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