TEST 4- STUDY GUIDE 3 Flashcards
Parkinson’s- What are the 3 cardinal manifestations of Parkinson’s disease?
-Bradykinesia- slowness of movement
-Rigidity
-Rest tremor
What do patients with Parkinsons disease look like?
stooped posture:
-Cogwheeling
-tremor
-maslike face (hypomimia)
-soft speech (hypophonia)
- small, slow handwriting (micrographia)
-dysphagia
-cognitive decline
John, a 68-year-old man, presents to the clinic with complaints of difficulty in movement and maintaining balance. Over the past year, he has noticed a tremor in his right hand, especially at rest, and a significant reduction in his handwriting size. His family reports that he has developed a stooped posture and shows little facial expression. He occasionally experiences moments of confusion and mild hallucinations. John also reports ongoing issues with constipation and recent difficulty with speaking softly.
Question 1: Identifying Core Symptoms
Q: What are the core manifestations of Parkinson’s Disease observed in John’s presentation?
A: Bradykinesia, rest tremor, rigidity, stooped posture, hypomimia (masklike face), micrographia, and hypophonia.
Rationale: PD commonly presents with a combination of motor symptoms such as bradykinesia, rest tremor, and rigidity alongside additional features like hypomimia, hypophonia, and micrographia, all of which are observable in John’s symptoms.
*Q:** What non-motor symptoms associated with Parkinson’s Disease does John exhibit?
Constipation, soft speech (hypophonia), cognitive changes, confusion, and hallucinations.
Rationale: Non-motor symptoms, including autonomic dysfunction, cognitive decline, and psychiatric symptoms such as hallucinations, are prevalent in PD patients and can significantly impact the patient’s quality of life.
hich non-pharmacological strategies could potentially help manage some of John’s symptoms, such as constipation and balance issues?
A: Dietary modifications, increased fluid and fiber intake for constipation, physical therapy to improve balance and movement, and possibly speech therapy for hypophonia.
Rationale:** Implementing lifestyle changes and therapies can be beneficial in managing some aspects of PD. Physical therapy can help improve mobility and balance, while dietary changes often help relieve constipation issues.
Considering John’s hallucinations, why might it be important to review his current medication regimen?
A: Certain PD medications can contribute to or exacerbate hallucinations, necessitating a review to adjust doses or switch medications under medical guidance.
Rationale:** Medication-induced hallucinations are common in PD, particularly with dopaminergic treatments. Adjusting these treatments could help manage these psychiatric symptoms.
How might autonomic dysfunction be further evaluated in John to clarify its extent, especially given his bowel and bladder symptoms?
A: Comprehensive questioning about urinary habits, thorough review of bowel movement patterns, clinical tests for orthostatic hypotension, and possible referral to gastroenterology or urology.
Rationale:** Evaluating the full scope of autonomic dysfunction is important for overall management, involving direct inquiry, clinical examination and specialist input if necessary.
True or False many patients with Parkinsons disease exhibit behavioral changes?
True:
-apathy
-anxiety
-depression
-agitation
-hallucinations
Common problems in parkinsons disease?
-constipation
-bladder dysfunction
-sexual dysfunction
orthostatic hypotension
What are the core manifestations of Parkinson’s Disease observed in John’s presentation?
A: Bradykinesia, rest tremor, rigidity, stooped posture, hypomimia (masklike face), micrographia, and hypophonia.
Rationale:** PD commonly presents with a combination of motor symptoms such as bradykinesia, rest tremor, and rigidity alongside additional features like hypomimia, hypophonia, and micrographia, all of which are observable in John’s symptoms.
What non-motor symptoms associated with Parkinson’s Disease does John exhibit?
A: Constipation, soft speech (hypophonia), cognitive changes, confusion, and hallucinations.
Non-motor symptoms, including autonomic dysfunction, cognitive decline, and psychiatric symptoms such as hallucinations, are prevalent in PD patients and can significantly impact the patient’s quality of life.
Manage some of John’s symptoms, such as constipation and balance issues?
A: Dietary modifications, increased fluid and fiber intake for constipation, physical therapy to improve balance and movement, and possibly speech therapy for hypophonia.
Rationale:** Implementing lifestyle changes and therapies can be beneficial in managing some aspects of PD. Physical therapy can help improve mobility and balance, while dietary changes often help relieve constipation issues.
Considering John’s hallucinations, why might it be important to review his current medication regimen?
A: Certain PD medications can contribute to or exacerbate hallucinations, necessitating a review to adjust doses or switch medications under medical guidance.
Rationale:** Medication-induced hallucinations are common in PD, particularly with dopaminergic treatments. Adjusting these treatments could help manage these psychiatric symptoms.
How might autonomic dysfunction be further evaluated in John to clarify its extent, especially given his bowel and bladder symptoms?
A: Comprehensive questioning about urinary habits, thorough review of bowel movement patterns, clinical tests for orthostatic hypotension, and possible referral to gastroenterology or urology.
Evaluating the full scope of autonomic dysfunction is important for overall management, involving direct inquiry, clinical examination and specialist input if necessary.
Onset of Parkinsons disease
Preclinical stage [6]
Constipation
Anosmia
Sleep disturbances
REM sleep behavior disorder (RBD)
Restless leg syndrome
Excessive daytime sleepiness
Mood disorders (most commonly depression, apathy, and/or anxiety)
Parkinsonism TRAPs the patient: Tremor, Rigidity, Akinesia, and Postural instability.
Levodopa challenge test: performed to support the diagnosis of PD or as part of the evaluation prior to implantation of a deep brain stimulator
Parkinson’s Disease: Follow-up and Referral
Refer to specialist
As the disease progresses, especially in the area of tremor, it may become necessary to refer the patient to a movement disorder neurologist or to a stereotactic neurosurgeon to consider surgical treatment options, such as deep brain stimulation.
Rating scales are frequently used to evaluate and monitor a patient’s response to medications.
The Unified Parkinson’s Disease Rating Scale (UPDRS) is a comprehensive evaluation tool that assesses mental, historical, and motor features and the complications of dopaminergic therapy.
A subscale of the UPDRS is the Activities of Daily Living Scale, which assesses speech, salivation, swallowing, handwriting, cutting food, handling utensils, hygiene, turning in bed, falling, freezing, walking, tremor, and sensory symptoms
The ___ Scale (UPDRS) is a comprehensive evaluation tool that assesses?
**tools monitor the patients response to medications
Unified Parkinson’s Disease Rating Scale (UPDRS)
-Mental
-Historical
-Motor features
-Complications of dopaminergic therapy
What is the sub scale of the UPDRS is the___
Activities of Daily Living scale (parkinson disease evaluation)
-speech
-salivation
-swallowing
-handwriting
-cutting food
-handling utensils
-hygiene
-turning in bed
-falling
-freezing
-walking
-tremor
-sensory symptoms
When should a patient with Parkinson’s Disease be referred to a movement disorder specialist or a stereotactic neurosurgeon?
A. When there is a first diagnosis of Parkinson’s Disease.
B. When non-motor symptoms such as constipation appear.
C. When dopaminergic medications no longer control symptoms effectively or if surgical options like deep brain stimulation are considered.
D. When initial symptoms of tremor and rigidity are first observed.
*Answer:** C. When dopaminergic medications no longer control symptoms effectively or if surgical options like deep brain stimulation are considered.
Rationale: Referral to a specialist or neurosurgeon is typically indicated when the patient’s symptoms are not adequately managed by medications alone, and surgical interventions might be explored to alleviate symptoms such as tremor.
Which rating scale is specifically used to evaluate and monitor a patient’s response to Parkinson’s medications and assess mental, historical, and motor features?
A. Montreal Cognitive Assessment (MoCA)
B. Mini-Mental State Examination (MMSE)
C. Unified Parkinson’s Disease Rating Scale (UPDRS)
D. Geriatric Depression Scale (GDS)
Answer:** C. Unified Parkinson’s Disease Rating Scale (UPDRS)
Rationale: The UPDRS is a subjective and objective tool specifically designed for comprehensive assessment of Parkinson’s Disease, including response to medications, mental status, motor skills, and complications.
The Activities of Daily Living Scale, a subscale of the UPDRS, assesses which of the following activities?
A. Cognitive functions and memory
B. Sleep patterns and anxiety levels
C. Speech, salivation, swallowing, and handling utensils
D. Vision acuity and hearing ability
*Answer:** C. Speech, salivation, swallowing, and handling utensils
Rationale: The Activities of Daily Living Scale within the UPDRS focuses on practical and physical tasks that can be significantly impacted by Parkinson’s Disease, such as speaking, swallowing, personal hygiene, and using utensils.
Aside from motor symptoms, Parkinson’s Disease often presents with autonomic dysfunctions. Which symptom is NOT typically associated with autonomic dysfunction in Parkinson’s Disease?
A. Constipation
B. Bladder dysfunction
C. Insomnia
D. Orthostatic hypotension
*Answer:** C. Insomnia
Rationale: While insomnia can occur in Parkinson’s due to other factors like medication side effects, it is not directly categorized under autonomic dysfunction, which includes symptoms like constipation, bladder issues, and orthostatic hypotension.
MAO- B medications
Delays the metabolism of dopamine - Correct.-inhibitors work by blocking the enzyme monoamine oxidase B, which breaks down dopamine, thus prolonging dopamine’s availability in the brain.
MAO-B inhibitors don’t directly activate dopamine receptors; they work by preventing dopamine breakdown.— THEY DO NOT TRIGGER DOPAMINE RECEPTORS
MAO-B inhibitors- inhibit dopamine metabolism.
MAO-B MEDICCATIONS TRUE OR FALSE
Converts levodopa to dopamine - Incorrect. This is the function of dopa decarboxylase, not MAO-B inhibitors.
FALSE
MAO-B inhibitors delay the metabolism of dopamine. WE DO NOT WANT DOPAMINE TO BE METABOLIZED BECAUSE DOPAMINE HELPS IN FUNCTION. SO THE DELAY IS A GOOD THING
This mechanism helps maintain higher dopamine levels in the brain, which is beneficial for Parkinson’s Disease patients who have depleted dopamine levels.
This mechanism helps maintain higher dopamine levels in the brain, which is beneficial for Parkinson’s Disease patients who have depleted dopamine levels.
Identify a drug that inhibits MAO-B to slow the metabolism of dopamine in the brain?
1. Rasagilline
2. Bromocriptine
3. Carbidopa
4. Tolcapone
5. Levodopa
Rasagiline is a drug that inhibits monoamine oxidase-B (MAO-B) to slow the metabolism of dopamine in the brain.
By doing so, it can help manage the symptoms of Parkinson’s disease and related movement disorders by increasing the availability of dopamine and reducing motor symptoms.
Rasagiline is often used alongside other medications and therapies as part of a comprehensive treatment plan aimed at improving the quality of life for those living with Parkinson’s disease and related conditions.
What is the class of these medications?
Rasagilline
- MAO-B Inhibitors
Bromocriptine class of med?
Dopamine receptor agonists.
It treats hyperprolactinemia by decreasing the amount of prolactin in the body. It treats acromegaly by decreasing the amount of growth hormone in the body.
It treats Parkinson’s disease by stimulating the nerves that control movement.
Rasagiline belongs to a class of medications called MAO-B inhibitors, which are used to manage the symptoms of Parkinson’s disease and other related movement disorders.
The drug works by selectively inhibiting MAO-B, preventing the breakdown of dopamine and increasing its availability in the brain.
This helps to alleviate the motor symptoms associated with low dopamine levels, such as tremors, rigidity, and bradykinesia (slowness of movement).
What class is carbidopa?
Dopaminergic Medications
What drug class is Tolcapone?
Catechol-O-methyl transferase inhibitor class of drugs. (COMT)
What drug class is levodopa?
Dopamingeric Medication
L-DOPA (Levodopa) in Parkinson’s Disease Treatment
L-DOPA (levodopa) is a precursor to dopamine that, unlike dopamine itself, can cross the blood-brain barrier. Once in the brain, it’s converted to dopamine by DOPA decarboxylase in presynaptic neurons, primarily activating D2 receptors.
Key characteristics?
Most effective medication for reducing Parkinson’s disease symptoms, particularly bradykinesia (slow movement)
Typically first-line treatment, especially for older patients
Usually administered with decarboxylase inhibitors (like carbidopa) to reduce peripheral conversion and side effects
Should be taken between meals (30 minutes before eating) to improve absorption, as high-protein foods can interfere with uptake
What are side effects of levodopa?
Immediate: nausea, vomiting, orthostatic hypotension (reduced by carbidopa)
Psychiatric: hallucinations, anxiety
Motor complications with long-term use: hypokinesia (reduced movement), dyskinesia (involuntary movements), and potentially akinetic crisis (severe immobility)
The primary challenge with L-DOPA is that while initially highly effective,
long-term use often leads to motor complications that can significantly impact quality of life, creating a treatment dilemma in Parkinson’s management.
Which of the following statements best describes how Levodopa helps to manage the motor symptoms of Parkinson’s disease?
a.
Levodopa is synthesised in the brain into dopamine resulting in dyskinesia to counteract the bradykinesic symptoms.
b.
Levodopa crosses the blood-brain barrier and is converted to dopamine resulting in an improvement in symptoms.
c.
Levodopa is unable to cross the blood-brain barrier so prevents further increases in dopamine resulting in and improvement in symptoms.
d.
Levodopa blocks the conversion of dopamine resulting in an improvement in symptoms.
b. Levodopa crosses the blood-brain barrier and is converted to dopamine resulting in an improvement in symptoms.
Levodopa is a prodrug that is converted to dopamine by DOPA decarboxylase and can cross the blood-brain barrier. When in the brain, levodopa is decarboxylated to dopamine and stimulates the dopaminergic receptors, thereby compensating for the depleted supply of endogenous dopamine seen in Parkinson’s disease.
MAO-B inhibitors (such as selegiline and rasagiline) are monoamine oxidase inhibitors. This means that they inhibit the breakdown of dopamine in the brain. This allows L-DOPA to be more effective and to last longer.
L-DOPA (levodopa) is an important medication in the treatment of Parkinson’s Disease. Why is it used instead of dopamine, and how can its effectiveness be extended using other drugs?
is used to instead of dopamine because dopamine itself does not cross the blood - brain barrier . is a precursor to dopamine ,which means that it is converted to dopamine once it enters the brain. This allows to increase dopamine levels in the brain, which is necessary to treat the symptoms of parkinson’s disease.
How to extend the effectiveness of L-DOPA using other drugs:
Explanation:
There are a number of drugs that can be used to extend the effectiveness of . These drugs work in different ways, but they all aim to increase the amount of that reaches the brain and/or to slow down its breakdown.
COMT inhibitors (such as entacapone and tolcapone) are inhibitors. This means that they inhibit the breakdown of dopamine and
L-DOPA risk of ?
severe motor dysfunction. with longterm use
What is the function of L-DOPA?
is converted to dopamine by DOPA decarboxylase at the presynaptic neuron → direct dopaminergic effect (especially at D2 receptors)
L-DOPA, in contrast to dopamine, can cross the blood-brain barrier.
Predominantly controls bradykinetic symptoms
Initial treatment option for most patients with PD, especially older patients?
levodopa
What are some adverse effects of dopamingeric medications? Levodopa
-Nausea
-H/A
-Orthostatic hypotension
-Confusion
-hallucinations
-peripheral edema
-compulsive behavior
Administer between meals (e.g., 30 minutes before a meal) to increase gastrointestinal absorption (→ avoid high-protein diets)
Decarboxylase inhibitors
Carbidopa
Benserazide
Always administered alongside L-DOPA
COMT inhibitor monotherapy is ineffective; therefore, it should always be combined with L-DOPA and carbidopa.
NMDA antagonists
Amantadine
Drug of choice during akinetic crisis
Anticholinergic agents
Benztropine
Trihexyphenidyl
Biperiden
Useful as monotherapy in patients < 65 years of age with tremor as the main symptom
Beneficial regarding tremor and rigidity but does not improve bradykinesia
Usually avoided in patients > 65 years because they are more prone to anticholinergic side effects (e.g., urinary retention, delirium, constipation)
To remember that anticholinergics like benztropine and trihexyphenidyl are used in the treatment of Parkinson disease, think of “A Benz for a trip to the park.”
To remember the main drugs used to treat Parkinson disease, think of A2 B2 C2 D2: Antimuscarinics and Amantadine; Bromocriptine and MAO-B inhibitors; COMT inhibitors and Carbidopa; L-DOPA and nonergot Dopamine agonists.
Open-angle glaucoma: Levodopa (and anticholinergics) should be used with caution.
Closed-angle glaucoma: Levodopa (and anticholinergics) are not recommended.
Akinetic crisis
Definition: condition caused by severe dopamine deficiency (e.g., after discontinuation of L-DOPA therapy or insufficient L-DOPA absorption)
Clinical features: complete inability to move , incomprehensible speech, possibly hyperthermia → increased risk of dehydration, deep-vein thrombosis, and pneumonia
Treatment: intensive medical care, volume substitution, administration of L-DOPA, apomorphine, amantadine
Levodopa (L-DOPA), a dopamine precursor, is the most effective medication for controlling the motor symptoms of Parkinson disease. Primary effects of L-DOPA are achieved by stimulating D2-receptors in the substantia nigra and striatum. However, overstimulation of D2-receptors by levodopa may also induce psychosis and hallucinations (usually visual). The risk for developing psychiatric symptoms increases with age, other psychiatric conditions, long duration of levodopa treatment, and high doses. Since this patient has been taking levodopa for 3 years and is elderly, her symptoms are most likely the result of levodopa therapy.
Other adverse effects of L-DOPA therapy include dizziness, somnolence or insomnia, anxiety, and aggressive behavior.
Trihexyphenidyl is a muscarinic antagonist that reduces cholinergic activity in the CNS. Initial monotherapy with an anticholinergic (e.g., trihexyphenidyl, benztropine, biperiden) can be considered in patients with PD who are ≤ 65 years of age if the main symptom is resting tremor and there is no evidence of cognitive impairment, significant bradykinesia, or gait disturbance.
Alternative pharmacotherapy for patients with PD who are ≤ 65 years of age includes nonergot dopamine agonists, MAO-B inhibitors, COMT inhibitors, and/or levodopa/carbidopa.
Anticholinergics should be avoided in patients > 65 years of age (particularly those with dementia) because they may worsen psychiatric symptoms and cause urinary retention.
Propranolol is a first-line treatment of benign essential tremor.
This patient likely has a family history of essential tremor (his father developed head bobbing at an older age). However, unlike the asymmetric resting tremor seen in this patient, essential tremor is symmetrical, worsens with voluntary movements, and resolves completely at rest.
Amantadine is a weak NMDA receptor antagonist that can improve motor symptoms (tremor, rigidity, akinesia) in patients with mild forms of Parkinson disease, or it can be combined with levodopa to reduce dyskinesia in patients with advanced disease. Livedo reticularis and peripheral edema, which are seen in this patient, occur as adverse effects in up to 5% of patients who take amantadine
A non-ergot dopamine agonist such as pramipexole or ropinirole is the typical first-line treatment for Parkinson disease in young patients (< 65 years) without cognitive impairment.
If symptoms are severe, combination treatment of levodopa with carbidopa and/or a COMT inhibitor (e.g, entacapone) can be initiated. Levodopa is more effective than dopamine agonists. However, levodopa therapy is usually reserved for elderly patients or patients with cognitive impairment.
MAO-B inhibitors (e.g., selegiline) or amantadine can be used as monotherapy in patients with minimal symptoms that do not affect quality of life, or as an adjunct with dopamine agonists or levodopa in more severe cases.
Direct dopamine receptor agonists (e.g., pramipexole, ropinirole) are the first-line treatment for Parkinson disease patients < 65 years of age. They are, however, associated with the development of impulse control disorders (e.g., compulsive gambling, hypersexuality, excessive spending of money), which occurs in up to 50% of patients with long-term use.
This adverse effect is presumably due to decreased neuronal activity in brain areas responsible for impulse and inhibitory control. Risk factors include high doses, long duration of treatment, young age, and male sex. Other common side effects of dopamine agonists include nausea, drowsiness, orthostatic hypotension, confusion, and hallucinations.
Patients may also develop compulsive use of these drugs (termed dopaminergic dysregulation syndrome). A withdrawal syndrome resembling cocaine withdrawal (e.g., anxiety, depression, sweating, nausea, fatigue, and drug craving) may occur if the drug is abruptly discontinued.
Entacapone is a peripherally acting COMT inhibitor that reduces the methylation of levodopa and dopamine, thus allowing a more stable and long-lasting plasma concentration of the drug.
This results in fewer periods of end-of-dose akinesia and less variability of symptoms during the day. Tolcapone is a centrally acting COMT inhibitor that is used for refractory Parkinson disease.
Motor fluctuations increase during long-term therapy with levodopa because the neurons gradually lose their capacity to store and release dopamine. The severity of symptoms is directly related to the drug dose.
Following administration, L-DOPA is absorbed into the systemic circulation where it is partially converted to dopamine by the enzyme DOPA decarboxylase. The remaining L-DOPA is then transported across the blood-brain barrier and enters the central nervous system to produce the desired effects.
Carbidopa reduces the peripheral (systemic) conversion of L-DOPA to dopamine, thereby mitigating the peripheral
side effects, including orthostatic hypotension, nausea, and vomiting. Although the combination of carbidopa-levodopa significantly improves drug compliance, many patients still experience some degree of these side effects.
Amantadine increases dopamine release, decreases dopamine reuptake, and inhibits the N-methyl-D-aspartate (NMDA) receptor. It can be used as initial short-term monotherapy in patients with mild symptoms of Parkinson disease, mainly for those with prominent tremor.
amantadine is associated with anticholinergic-like side effects (e.g., dry mouth, constipation), prolonged QT interval, and psychological disorders (e.g., hallucinations, anxiety).
DAs) such as ropinirole may lead to impulse control disorders (ICDs), irrespective of the underlying disease. Patients taking DAs should be aware of this adverse effect and regularly monitored, because ICDs may have debilitating effects on their work and social functioning. If the patient shows signs of ICDs, the dose should be slowly tapered or discontinued until symptoms resolve.
Abrupt discontinuation of DAs can lead to dopamine agonist withdrawal syndrome. Although most patients with ICDs due to DA therapy respond well to discontinuation of the medication, ICDs may persist in some patients.
Other adverse effects of DAs include restlessness, nausea, orthostatic hypotension, drowsiness, hallucinations, and psychosis.
-Doapa- (gel form to use with gastrostomy tube)
Dopaminergic Medications
-Parcopa- (oral dissolving tablet)
Dopaminergic Medications
Inbrija (inhaled)
Dopaminergic Medications
This med can be used as a rescue medication
For dopaminergic medications what med should be used if there is a swallowing dysfunction?
Parcopa (oral disintegrating tablet)
What are some adverse effects of dopamine agonists?
Pramipexole (mirapex)
Ropinirole
Apomorphine
-nausea
-sleepiness
-orthostatic hypotension
-confusion
-hallucinations
-peripheral edema
-compulsive behavior
What dopamine agonist can be used as a rescue therapy for its quick onset of action?
apomorphine
What meds are only beneficial with carbidopa/levodopa & with motor functions that wear off?
emtacapone (Comtan)
opicapone (omgentys)
What are some side effects of COMT inhibitors?
-diarrhea
-orange urine
**can worsen adverse effects of levodopa
What are adverse effects of anticholinergic drugs?
Trihexypenidyl
benzotropine mesylate
-confusion
-hallucinations
-dry mouth
-urinary retention
Side effects of antiviral medications?
amantadine
unknown mechanism of action in PD
can treat dyskinesia
-ankle edema
-confusion
-hallucinations
What migraine triptan medication is used as an injection and nasal spray?
Imitrex
When should triptans not be used?
Ischemic heart disease or cardiovascular disease
What are some side effects of triptans?
-paresthesia
-asthenia
-nausea
-dizzness
-neck or chest tightness
-heaviness
-somnolence
When should you not use ergot meds?
-PVD
-CAD
-HTN
-hepatic
-renal disease
The ergot med migranal is also available as a ?
nasal spray
IV route preferred for fast acting relief
NSAIDS risk factor?
mild to moderate pain, GI bleed with alcohol
Combo analgesics
not 1st line for treatment of migraines -drowsiness, dizziness, GI
butalbital
Opiates
sedation
resp failure
constipation
addiction
Medrol dose pack
dexamethasone IM/IV
adjunct therapy for severe refractory migraine headaches
beta blockers
preferred HTN, angina
Do not use in asthma
sinus bradycardia
2nd or 3rd AV block
increased by alcohol
causes weight loss
asthenia
mental fuzziness
antidepressants
-venlafaxne
nortriptyline
amitryline
can cause sedation- amitryline nighttime dosing
Calcium channel blocker verapamil
takes a long time (several months to be effective)
DO NOT USE IN PREGNANCY
side effects:
-somnolence
-dizziness
-asthenia
give seizure disorders and diabetic peripheral neuropathy
Resting tremor
action tremor
intention tremor
Benign essential tremor what is the best treatment?
1st propranolol line agent
then primidone- sedative hypnotic drug barbiturate
first line medications. All medications are started at a low dose and titrated to achieve the desired effect; the effective dose varies widely between patients.
Propranolol
DOSAGE. Some authors recommend a starting dose of 20 mg twice daily or 10 mg twice daily in older adults.
Primidone
DOSAGE. Some authors recommend a starting dose of 25 mg once daily at bedtime for older adults.
Alternative medications (if propranolol and primidone are ineffective or contraindicated)
Other beta blockers (e.g., atenolol, metoprolol)
Other anticonvulsants (e.g., topiramate, gabapentin)
Benzodiazepines (e.g., alprazolam, clonazepam)
beta blockers can mask symptoms of hypoglycemia
hyperlipidemia
weight gain
propranolol treats akathisia inability to sit still.
contraindications of propranolol
Symptomatic bradycardia
Cardiogenic shock and hypotension
Pheochromocytoma: administration of beta blockers before alpha blockers → unopposed α-adrenoceptor mediated vasoconstriction → hypertensive crisis (except nonselective beta blockers with α-antagonism, such as carvedilol and labetalol)
Decompensated heart failure
Combination with calcium channel blockers (diltiazem or verapamil): can precipitate AV block
Sick sinus syndrome (without a pacemaker); heart block greater than first-degree
