Clinical Pharmacy

Ruanee G. Escala, RPh, PharmD | Midterms | PHCLIN330

GABA ENHANCERS
Topic Outline: • Benzodiazepines, Valproic Acid
● Epilepsy
● Migraine TREATMENT ALGORITHMS
● Pain Management
DIAGNOSIS AND SEIZURE CLASSIFICATION
EPILEPSY • Determine if seizures are focal, generalized, or
• Neurological disorder characterized by unknown onset.
recurrent, unprovoked seizures. Epilepsy • Identify the epilepsy syndrome
happens as a result of abnormal electrical brain
activity, also known as a seizure, kind of like an FIRST-LINE THERAPY
electrical storm inside the head (Mayo Clinic) • Initiate monotherapy with an AED appropriate for
seizure type.
AFFECTED BRAIN REGIONS
• Focal (specific area) DOSE TITRATION AND MONITORING
• Generalized (entire brain) • Gradually increase the dose while monitoring for
efficacy and side effects.
SYMPTOMS
• Temporary confusion SECOND-LINE THERAPY
• A staring spell • If first AED fails, switch to another monotherapy
• Stiff muscles or considercombination therapy.
• Uncontrollable jerking movements of the arms
and legs SURGICAL AND NON- PHARMACOLOGICAL OPTIONS
• Loss of consciousness • For refractory cases, consider surgical
• Psychological symptoms such as fear, anxiety or intervention, neurostimulation, or dietary
deja vu therapy.

MECHANISM NON-PHARMACOLOGICAL TREATMENTS

• Caused by abnormal, excessive electrical
discharges in the brain LIFESTYLE MODIFICATIONS
• Disruption in the balance between excitatory • Avoiding seizure triggers (sleep deprivation,
(glutamate) and inhibitory (GABA) stress).
neurotransmission.
• Genetic predisposition, ion channel dysfunction, KETOGENIC DIET
and neuroinflammatory changes may contribute. • High-fat, low-carb diet shown to reduce seizure
frequency in some patients.
DRUG CLASSES IN EPILEPSY
ANTIEPILEPTIC DRUGS (AEDS) SURGICAL TREATMENT
• Resection of epileptic focus or corpus
SODIUM CHANNEL BLOCKERS callosotomy.
• Phenytoin, Carbamazepine
NEUROSTIMULATION
CALCIUM CHANNEL BLOCKERS • Vagus nerve stimulation (VNS) or responsive
• Ethosuximide (absence seizures) neurostimulation (RNS)

MIXED MECHANISM AGENTS PSYCHOSOCIAL SUPPORT

• Lamotrigine, Levetiracetam • Counseling, support groups, and educational
programs for patients and families.
GLUTAMATE INHIBITORS
• Topiramate, Felbamate

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Clinical Pharmacy
Ruanee G. Escala, RPh, PharmD | Midterms | PHCLIN330

HEADACHES MIGRAINE AND TENSION - TYPE ANTICONVULSANTS

• e.g., Topiramate
MIGRAINE • modulate neuronal firing
• Neurovascular disorder characterized by
changes in brainstem activity and CALCIUM CHANNEL BLOCKERS
neurotransmitter release. • e.g., Verapamil
• Involves activation of the trigeminovascular • reduce vasodilation
system, leading to release of inflammatory
mediators (e.g., CGRP, Substance P). ANTIDEPRESSANTS
• Cortical spreading depression (CSD) may trigger • e.g., Amitriptyline modulate serotonin and
aura and headache onset. norepinephrine
• Hypersensitivity in pain pathways contributes to
photophobia, phonophobia, and other sensory DRUG CLASSES
sensitivities.
ACUTE TREATMENT
TENSION-TYPE HEADACHE(TTH)
• Mechanism less defined; thought to involve NSAIDs
heightened sensitivity of peripheral pain • e.g., Aspirin, Ibuprofen
pathways and muscle tension. • reduce inflammation and pain
• Often associated with stress, anxiety, and
musculoskeletal strain. ACETAMINOPHEN
• Central sensitization may occur in chronic TTH. • analgesic effect

DRUG CLASSES PROPHYLACTIC TREATMENT

ACUTE TREATMENT TRICYCLIC ANTIDEPRESSANTS

• e.g., Amitriptyline
TRIPTANS • reduce central pain sensitization.
• e.g., Sumatriptan
• 5-HT1B/1D receptor agonists, inhibit neurogenic TREATMENT ALGORITHM
inflammation
MIGRAINE
NSAIDs • Start with NSAIDs or acetaminophen for mild
• e.g., Ibuprofen attacks.
• reduce inflammation and pain • Moderate to severe: Use triptans or combination
therapy (triptan + NSAID).
ERGOT ALKALOIDS • Consider prophylactic therapy if: =4
• e.g., Ergotamine headaches/month
• vasoconstriction and 5-HT receptor agonism • Debilitating attacks.
• CGRP antagonists or botulinum toxin for chronic
CALCITONIN GENE-RELATED PEPTIDE (CGRP) cases.
ANTAGONISTS
• e.g., Rimegepant TENSION-TYPE HEADACHE
• block CGRP, a key migraine mediator • Acute: NSAIDs or acetaminophen.
• Chronic: Consider prophylactic treatment with
PROPHYLACTIC TREATMENT tricyclic antidepressants.
• Address comorbid anxiety and stress
BETA-BLOCKERS management.
• e.g., Propranolol
• reduce excitability of the central nervous system

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Clinical Pharmacy
Ruanee G. Escala, RPh, PharmD | Midterms | PHCLIN330

NON-PHARMACOLOGICAL TREATMENT Opioid Analgesics

• Medications like Morphine and Fentanyl are
Lifestyle Modifications reserved for moderate to severe pain but carry
• Regular sleep, hydration, balanced diet, and risks of tolerance and dependence.
exercise.
Anticonvulsants
Behavioral Therapies • Drugs like Gabapentin and Pregabalin reduce
• Cognitive Behavioral Therapy (CBT). neuropathic pain by stabilizing nerve activity.
Biofeedback and relaxation techniques. Stress
management and coping strategies. Antidepressants
• Tricyclic antidepressants and SNRIs such as
Physical Therapy Amitriptyline and Duloxetine are effective for
• Postural correction and neck exercises (for neuropathic pain.
TTH).
Muscle Relaxants
Acupuncture and manual therapy. • Used for conditions involving muscle spasms,
• Avoidance of Triggers such as Baclofen or Cyclobenzaprine.
• Identify, avoid specific triggers (food, stress,
environmental factors). Corticosteroids
• Anti-inflammatory agents like Prednisone are
PAIN MANAGEMENT useful in reducing inflammation and associated
• Pain is a multifaceted experience with both pain.
sensory and emotional components, originating
from tissue damage or the potential for it. The Topical Analgesics
process involves four key phases. • Lidocaine patches and Capsaicin creams target
localized pain.
TRANSDUCTION
• Nociceptors detect harmful stimuli and convert PAIN MANAGEMENT ALGORITHM
them into electrical impulses.
Mild Pain (1-3)
TRANSMISSION • Initiate treatment with non-opioid medications
• Pain signals travel from the injury site via (e.g., Acetaminophen, NSAIDs).
peripheral nerves to the spinal cord and then to
the brain. Moderate Pain (4-6)
• Combine non-opioids with weak opioids (e.g.,
PERCEPTION Tramadol) and consider adjuvants like
• The brain processes these signals, leading to the antidepressants.
conscious experience of pain.
Severe Pain (7-10)
MODULATION • Strong opioids (e.g., Morphine) are used in
• The body either amplifies or dampens pain combination with adjunctive therapies (e.g.,
through descending pathways that release nerve blocks or ketamine in severe cases).
neurotransmitters like serotonin or
norepinephrine. Chronic Pain
• Begin with non-opioids and consider
DRUG CLASSES antidepressants and anticonvulsants. Opioids
are reserved for severe, intractable pain.
Non-Opioid Analgesics
• Acetaminophen and NSAIDs are typically used
for mild pain and inflammatory conditions.

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Clinical Pharmacy
Ruanee G. Escala, RPh, PharmD | Midterms | PHCLIN330

NON-PHARMACOLOGIC PAIN MANAGEMENT

Physical Therapy
• Improves mobility and reduces pain through
targeted exercises.

Cognitive Behavioral Therapy (CBT)

• Helps patients manage pain by addressing
psychological factors.

Acupuncture and TENS

• These methods aim to modulate pain perception
by stimulating specific points on the body or
using electrical impulses.

Heat/Cold Therapy
• Used to reduce inflammation or relax muscles,
depending on the nature of the pain.

Chiropractic Care
• Focuses on manual manipulation of the spine to
alleviate pain.

Mindfulness and Meditation

• Mental techniques to reduce the emotional
impact of pain.

Yoga
• Integrate movement and mindfulness to improve
flexibility and reduce pain perception.