Impact of drug therapy on various neurological conditions and its effects on rehabilitation; conditions like stroke, parkinson's disease,vertigo and also its effects on various impairments like spasticity, sensory impairments, cognition

1. IMPACT OF DRUG THERAPY ON
PATIENT’S RECEIVING
NEUROLOGICAL REHABILITATION
Dr. Shweta Kotwani; Pediatric Physical Therapist
BPTh (MUHS); MPT (Neuro,MUHS); LASHS-U.K.
Fellowship Dip.(Peds.Rehab.; Clinical Neuro.Sc.)

2. Drug Therapy
• Whereas mono-therapy (the use of one drug
for treatment of a single disease state) is
preferred, complex pathologies and co-morbid
conditions usually render this goal impossible.
• Drugs used for the management of a wide
variety of disease states may have unintended
or undesirable effects on a therapeutic plan
for a client undergoing neurological
rehabilitation.

3. Clinical Pharmacology
• Medications do not affect all clients in the same way, and
rehabilitation specialists should be concerned whether a
drug achieves or falls short of achieving its therapeutic
response.
• Many situations may alter a drug’s response, including drug
dose, drug interactions, and a client’s co-morbidities, and
the effect on functional recovery can be positive or
negative.
• Pharmacology—or the science of drug origin, nature,
chemistry, effects, and uses—is commonly divided into two
important areas:
• Pharmacokinetics
• Pharmacodynamics.

4. Impairment Perspective
• Sensory impairments
• Motor Problems
• Cognitive deficits
• Problems with balance and co-ordination
• Cardiovascular impairments
• Problems with muscle tone
• Neuroplasticity

5. Sensory impairments
• In any impairment, the processing of accurate sensory
information is crucial to modify and adjust procedural
programming during movement, will affect the motor
performance.
• Reflex arc
• Clients with sensory integrative problems are often
given medications such as those for attention-deficit
disorder, anxiety, seizure, and depression.
• Certain drugs may influence hearing or produce
tinnitus (e.g., aspirin), changes in the visual field (eg.
with ethambutol and anticonvulsants) which may be
distracting and thus ultimately affect motor
performance.

6. Sensory impairments
• Analgesics and topical anesthetics may dangerously
affect surface heat or cold discomfort. However,
elimination of excessive pain (peripheral and central)
may enhance cognitive focus and learning as well as
allow an individual to move as part of daily living,
which will help maintain power, range, balance, and
thus quality of life.
• The peripheral effects of drugs commonly modify the
function of central systems. Drug therapy can modify
rehabilitation techniques both positively and
negatively.

7. Sensory impairments
• Therapists must be aware of medications when
working with clients who have sensory
impairments.
• Medications can increase or alleviate signs and
symptoms, as well as produce unwanted side
effects.
• Clients may benefit from alterations in the
environment to limit sensory sensitivities, timing
of treatment to coincide with the most effective
dose of medications, and monitoring for
unwanted side effects.

8. Cognitive and central motor control
impairment
• Disorders of mood (anxiety and depression)
reduce initiative in the rehabilitation process.
• Anxiolytics and antidepressants- positive impact.
• Benzodiazepines and antidepressants- same
effects
• Behavioral disorders, especially those associated
with untreated psychoses or dementia, impede
cognitive function; antipsychotics may correct
these disorders.
• The dopaminergic antagonism associated with
antipsychotics may interfere with the function of
the basal ganglia and facilitation of movement

9. Cognitive and central motor control
impairment
• Many newer antipsychotic agents (also known as
the atypical antipsychotics) have, in addition to
dopaminergic antagonism, serotonin antagonist
activity, which may reduce the extrapyramidal
side effects of the earlier agents when analyzed
as movement dysfunction.
• The therapist should be monitoring for signs of
depression, which is common in clients who have
had loss of function.
• Extrapyramidal motor signs should be monitored
and reported to the health care team.

10. Examples of antipsychotic agents
• Standard Antipsychotics-
• Chlorpromazine (thorazine)
• Fluphenazine (Prolixin)
• Haloperidol (Haldol)
• Loxapine (Loxitane)
• Molindone (Moban)
• Atypical Antipsychotics-
• Asenapine (Saphris)
• Clozapine (Clozaril)
• Risoeridone (Risperdal)

11. Vertigo, Dizziness, Balance and
Co-ordination
• Medications should be reviewed in all patients
with dizziness, as numerous medications can
be associated with this effect, including
alcohol and other CNS depressants,
aminoglycoside antibiotics, anticonvulsants,
antidepressants, anti-hypertensives,
chemotherapeutics, loop diuretics, and
salicylates.

12. Vertigo, Dizziness, Balance and
Co-ordination
• Clients should be monitored for orthostatic
hypotension and hyperventilation.
• Depending on the cause of dizziness, clients with
dizziness may benefit from canalith repositioning
procedures, vestibular exercises, instrumental
rehabilitation training on a moving platform,
positional education (sitting at bedside before
standing), use of compression garments, dietary
changes (salt and fluid intake), and use of simple
physical counter-maneuvers such as squatting to
temporarily but rapidly raise blood pressure.

13. Cardiovascular impairments
• In the management of hypercholesterolemia, the 3-
hydroxy- 3-methylglutaryl coenzyme A (HMG-CoA)
reductase inhibitors may produce myopathies to various
degrees.
• Changes in hemodynamics caused by antihypertensive
regimens must be monitored because these agents can
produce syncope and lower exercise tolerance.
• Weakness from intermittent claudication is a challenge that
can be managed in part with cilostazol.
• Any drug that is used to decrease spasticity as a
consequence of stroke and related cerebrovascular
disorders may impair motor control and thus affect motor
learning.

14. Cardiovascular impairments
• Knowing the pharmacological management for
and side effects of medications related to the
cardiovascular system will assist the therapist in
providing high-quality care.
• Clients will benefit from education on modifiable
and non-modifiable risk factors, monitoring blood
pressure and heart rate, signs of heart failure,
vascular effects of modalities, and responses to
exercise and positional changes.

15. Spasticity and Muscle Tone
• Muscle spasms may be controlled with centrally acting and
peripherally acting agents, all of which produce drowsiness,
dizziness, and muscle weakness to various degrees.
• Tizanidine (Zanaflex) is the newest of the alpha-adrenergic agonists
available to reduce spasticity, primarily through activation of
descending noradrenergic inhibitory pathways.
• Clonidine (Catapres) has similar actions.
• Intrathecal administration of baclofen (Lioresal) produces an
antispasmodic effect through enhancement of GABAergic function,
both central and spinal.
• Likewise, enhancement of GABAergic function and reduced
spasticity can be realized through the anti-seizure drug gabapentin.

16. Spasticity and Muscle Tone
• Selective motor neurons can be inactivated through local
injection of botulinum toxins.
• These agents inhibit the release of acetylcholine at the
neuro- muscular junction. The investigational agent 4-
aminopyridine has been shown to reduce spasticity in
patients with spinal cord injury.
• Cyproheptadine, a relatively nonselective serotonergic
antagonist, can reduce spasticity and maintain muscle tone.
However, SSRIs used as antidepressants may occasionally
increase spasticity, and clozapine (Clozaril), a selective
serotonin antagonist, may produce muscle weakness.
• In addition to spinal cord injuries, multiple sclerosis (MS)
may cause spasticity as a complication.

17. Spasticity and Muscle Tone
• Although several interferons have been used
in the management of MS, interferon beta-1b
has been shown to increase spasticity
• Knowing the underlying cause of the spasticity
in the client with neurological impairments
(disruptions of inhibitory control) and using
concomitant rehabilitation therapy may assist
with decreasing pain and improving range of
motion and functional ability.

18. Spasticity and Muscle Tone
• baclofen (Lioresal)*
• carisoprodol (Soma)*
• chlorzoxazone (Paraflex)*
• cyclobenzaprine (Flexeril)*
• dantrolene (Dantrium)†
• metaxalone (Skelaxin)*
• methocarbamol (Robaxin)*
• orphenadrine (Norflex)*
• tizanidine (Zanaflex)*
• *Direct effects on motor systems to reduce tone.
†Direct effects on muscle to reduce tone.

19. Neuroplasticity
• In Alzheimer disease a loss of plasticity may occur
through deficits in hippocampal and cortical function,
leading to memory loss. Many anticholinesterase
agents improve memory, which may provide evidence
that they enhance neuroplasticity.
• Neuroprotective agents that aim to prevent neuronal
death by inhibiting one or more pathophysiological
steps in the process that follows brain injury or
ischemia are currently under development for
neurological disorders including stroke, spinal cord
injury, traumatic brain injury, and Parkinson disease.

20. Neuroplasticity
• In addition, studies on enriched environments
are providing knowledge related to neuronal
capacity for regeneration and repair in the
adult and ageing brain and spinal cord.
• The future of neuroplasticity in rehabilitation
may be enriched when medications that
protect or promote neurological recovery can
be paired with techniques to improve
function.

21. Disease Perspective
• Parkinson’s Disease
• Seizure Disorders (Epilepsy)
• Cancer
• Diabetes
• Infectious Diseases
• Stroke
• Autoimmune Disorders- similar to cancer
• Anxiety & Depression- mentioned in other
disorders
• Pulmonary Diseases

22. Parkinson’s Disease
• Parkinson disease is a degenerative disorder involving a
progressive loss of dopaminergic neurons in the substantia
nigra.
• This deficit in dopaminergic function results in resting
tremor, bradykinesia and rigidity.
• Cardiovascular function, bowel motility, and cognitive
function are often compromised.
• The functional deficits are emotionally devastating to the
patient, resulting in depression and other mood disorders.
• The predominant pharmacological approach in PD is the
enhancement of dopaminergic function in the affected
brain regions.

23. Parkinson’s Disease
• Levodopa (l-dopa), a precursor of dopamine in the central nervous
system (CNS)-only enhances the dopaminergic function in
remaining neurons.
• No effect on the progressive loss of neurons.
• In addition to central conversion of l-dopa to dopamine in the
substantia nigra, a similar conversion occurs in the limbic system, a
brain centre associated with the regulation of behaviour.
• Excessive dopaminergic influence in the limbic system has been
associated with aberrant behaviours, including paranoia, delusions,
hallucinations, and related psychiatric disturbances that may
influence sleep and mood. These behavioural changes are obviously
antagonistic to any therapeutic plan.

24. Parkinson’s Disease
• Agents converted to dopamine
• l-dopa (in Sinemet)
• Agents that stimulate release of dopamine
• amantadine (Symmetrel)
• Agents that reduce breakdown of dopamine
• carbidopa (in Sinemet)
• entacapone (Comtan)
• rasagiline (Azilect)
• selegiline (Eldepryl)
• tolcapone (Tasmar)
• Agents that are dopaminergic agonists
• apomorphine (Apokyn)
• bromocriptine (Parlodel)
• pergolide (Permax)
• pramipexole (Mirapex)
• ropinirole (Requip)
• Anticholinergic agents
• benztropine (Cogentin)
• diphenhydramine (Benadryl)
• trihexyphenidyl (Artane)
• The effects of these agents on muscle tone are complex and dose dependent

25. Parkinson’s Disease
• In the early months of the disease, the motor signs
may be particularly subtle, and patients may report
only slowness, stiffness, and trouble with handwriting.
• Particular attention to the history of tremor, slowness
of fine motor control, a hunched and slightly flexed
posture, and micrographia may lead the physician to
diagnose Parkinson disease in its early phases.
• As Parkinson disease advances, patients have
increasing difficulty in activities of daily living and gait
as well as bradykinesia and distal tremor.

26. Parkinson’s Disease
• The major problems that patients have after 5 years of treatment
for Parkinson disease are fluctuations (both motor and nonmotor),
dyskinesias, and behavioral or cognitive changes. Most commonly, a
predictable decline in motor performance occurs near the end of
each medication dose (“wearing off”).
• Patients change gradually from “on” with a good medication
response into an “off” period 30 minutes to 1 hour before the next
medication dose is due. Often patients have involuntary
movements (dyskinesias) as a peak-dose complication.
• Because these fluctuations occur throughout the day, accurate
detection requires the cooperation of the patient, who must be
trained to complete diaries of function. These journals generally
divide the 24-hour day into 30-minute segments to detect good
medication response (“on”), poor medication response (“off”),
disabling dyskinesias, and sleep.

27. Parkinson’s Disease
• In addition, clients should be monitored for postural hypotension,
dizziness, and cognitive changes.
• Therapists have the unique opportunity to determine the best
timing, frequency, and duration of the treatment, and
understanding the impact of a client’s drug regimen will only
enhance the outcome.
• Therapists must also be aware that exercise increases metabolism.
Increased metabolism may use up the medication faster; thus an
individual who generally remains symptom free (no off times
between doses) will again exhibit signs of the disease (distal
tremors and axial or proximal rigidity).
• These increases in symptoms may be a drug dosage problem, not
signs of further degeneration of the basal ganglia.

28. Seizure Disorders (Epilepsy)
• Epilepsy is associated with a diverse group of neurological disorders
resulting in motor, psychic, and autonomic manifestations.
• Many antiseizure medications may produce drowsiness, ataxia, and
vertigo. Although these adverse effects may be exhibited
throughout therapy, they are most troublesome during initiation of
drug therapy, addition of a drug, and dosage escalation.
• Sudden discontinuation of antiseizure medications may result in
status epilepticus, which may be fatal.
• Pharmacological adverse events that occur under the influence of
seizure medications must be recognized by the rehabilitation
specialist to participate in a team approach to patient care.
Therapists can assist in determination of effectiveness of a specific
treatment regimen, appropriate timing of rehabilitation
interventions, and the overall progress of the client during
rehabilitation.

29. Seizure Disorders (Epilepsy)
• Anticonvulsants
• acetazolamide (various brand names)
• carbamazepine (Tegretol)
• clonazepam (Klonopin)
• diazepam (Valium)
• ethosuximide (Zarontin)
• fosphenytoin (Cerebyx)
• gabapentin (Neurontin)
• lamotrigine (Lamictal)
• levetiracetam (Keppra)
• lorazepam (Ativan)
• oxcarbazepine (Trileptal)
• phenobarbital (various brand names)
• phenytoin (Dilantin)
• pregabalin (Lyrica)
• tiagabine (Gabitril)
• topiramate (Topamax)
• valproic acid (Depakene)
• Effects on motor systems are direct and may decrease tone at higher doses. Direct effects on muscle are
minimal. This list includes benzodiazepines that have antiseizure applications.

30. Seizure Disorders (Epilepsy)
• The practicing clinician working with clients who have a history of seizure
disorders must be prepared for the onset of a seizure and be aware of any
adverse side effects of medications.
• Many of the common side effects can also have negative implications for
motor learning, especially while the client is getting used to the
medication or the dosage is being elevated or tapered.
• The effects of the medications vary and may include enhancing the
inhibitory effects of γ-aminobutyric acid (GABA) (benzodiazepines);
reducing post-tetanic potentiation, thereby reducing seizure spread
(iminostilbenes); or modulating neuronal voltage-dependent sodium and
calcium channels (hydantoin).
• The overall result is a reduction in abnormal electrical impulses in the
brain.
• If seizures are recurrent and occur during critical periods of childhood,
adolescence, and early adulthood, they may result in significant
impairments in function and increased disability.

31. Valproic Acid
• One common antiseizure medication, valproic acid
(Depakene), may cause nausea, vomiting, hair loss,
tremor, tiredness, dizziness, and headache.
• Valproic acid has also been reported to aggravate
absence seizure in clients with absence epilepsy.
• Metabolic side effects may include an increase in
glucose-stimulated pancreatic insulin secretion, which
may be followed by an increase in body weight.
• Long-term valproic acid use is known to increase bone
resorption in adult epileptic patients and lead to a
decreased bone mineral density.

32. Other seizure medications
• Carbamazepine (Tegretol), is considered a safe drug but has a long
list of adverse events, most commonly ataxia and nystagmus.
• Gabapentin (Neurontin) is another well-tolerated antiseizure
medication with proven clinical efficacy and a low incidence of
adverse events in clinical trials. Common side effects include
dizziness, fatigue, and headache.
• Phenytoin (Dilantin) has adverse reactions including ataxia,
nystagmus, slurred speech, confusion, dizziness, and, at high doses,
peripheral neuropathy.
• Benzodiazepines (e.g., diazepam) are useful in managing status
epilepticus, but their effects are not long lasting so they are often
used along with a primary anticonvulsant. The most frequent side
effects are dose-related sedation, difficulty with concentration,
dizziness, and difficulty walking.

33. Cancer
• Disorders associated with abnormal and
uncontrolled cell growth.
• Any organ system in the body can be affected
either as the primary site of the disorder or a
secondary site associated with metastasis
• Tumors within the brain may interfere with
cognitive and motor function as well as
autonomic and metabolic control.
• Peripherally, tumors may interfere with
peripheral nerve function and associated motor
control or may produce pain.

34. Cancer
• Morphine, opiate derivatives- long-term
administration
• In cancer chemotherapeutic regimens-
antiemetic agents are used
• Dopaminergic antagonists-produce motor
deficits similar to PD
• Dronabinol-affects cognitive function
• High dose of corticosteroids-affects mood

35. Cancer
• Antitumor agents-neurotoxic-a reduction in deep
tendon reflex, paresthesias, demyelination-
Vincristine (Oncovin)
• Role of rehab specialist- help cancer patients
recover from the physical changes that
accompany their illness
• Promote function in ADL’s
• Help provide adaptations to activities within the
limits of each patient’s function and the illness
• Should be aware of chemotherapy and
medications-toxic effects and side effects.

36. Cancer
• Chemotherapy principle-agents that kill dividing cells will
kill tumor cells
• Tissues that rapidly divide-at risk- hair, mucosal lining, bone
marrow, immune cells, skin epithelial cells
• BRMs- non-chemotherapy medications- interferon and
interleukin.
• Exercise is thought to help improve endurance and
functional abilities
• Major side effects associated with BRMs-arthralgia and
myalgia
• Lymphedema-fluid retention caused by disruption of
lymphatic drainage or removal of lymph nodes.
• Suicidal ideation and depression-affects the QoL

37. Diabetes
• Disorder of insulin production and sensitivity
• Type 1- insulin dependent
• Type 2-non-insulin dependent
• Development of peripheral neuropathy-
progressive problem in patients with diabetes
• Acute problem- swings in blood glucose level
from inappropriate diet, exercise insulin and oral
hypoglycemic drug administration
• Swings in blood glucose level- changes in
behavior and sensorium
• Cognitive and motor function impaired

38. Diabetes
• An increase in exs intensity will decrease blood
glucose concentration thereby reducing insulin
requirements.
• Main goal of diabetes management- prevent both
small vessel complications (neuropathy) and large
vessel complications (amputation) of the disease
linked with elevated blood glucose levels.
• Diabetes is controlled through intensive
treatment regimens of diet, physical activity, oral
agents and insulin.
• Monitor hypoglycemia

39. Diabetes
• First step includes diet, physical activity, exercise
program to reduce body weight by 5% to 10%
• Vigorous exercise- glucose use can increase several fold
and this increase can persist long after the completion
of exercise- resulting in a fall in blood glucose. Thus
oral agents/insulin are required to achieve glycemic
control
• Five classes of oral agents- sulfonylureas
(chlorpropamide), meglitinides (repaglinide),
biguanides (metformin), glitazones (rosiglitazone) and
alpha-glucosidase inhibitors (acarbose)
• Effects- weight gain, GI symptoms, hypoglycemia

40. Diabetes
• Hypoglycemia- side effect in the rehab setting
because abnormally low glucose levels can cause
alterations in cognition, cardiovascular
hemodynamic changes and increased risk of
physical injury.
• Early signs of include shaking, sweating, fatigue,
weakness
• Later signs- confusion, exhaustion,
combativeness, inhibits eating, lead to loss of
consciousness

41. Diabetes
• American Diabetes Association (ADA)- guidelines
• Medical evaluation of the client before exs begins is important to
determine the extent of involvement and complications present
• Prepare the client for exercise by monitoring glycemic control before,
during and after exercise
• Exs in C/I if fasting glucose levels are more than 250 mg/dL and ketosis is
present
• Use caution if glucose levels are greater than 300mg/dL and no ketosis is
present.
• Patient should ingest added carbohydrate if glucose levels are less than
100mg/dL
• Document when changes in insulin or food intake are necessary and learn
glycemic response to different exercise conditions (light, moderate, heavy)
• Food intake should include consumption of carbohydrates as needed to
avoid hypoglycemia.
• Carbohydrate based food should be readily available during and after
exercise.

42. Infectious Diseases
• Both bacterial and viral diseases may produce
neurological disorders.
• In the course of treating bacterial diseases, many
antibiotic and anti-infective agents may
compromise sensory, motor and cognitive
function. (temporary/permanent, patient-
specific)
• In the critically ill patient, aminoglycosides
(gentamicin, tobramycin, amikacin) and
vancomycin may produce ototoxicity- hearing loss
(sensorineural and conductive) and vestibular
damage (dizziness, vertigo and ataxia)

43. Infectious Diseases
• Minocycline- vestibular toxicity
• Therapist should take extra precautions to
prevent falls during and after therapeutic exercise
sessions.
• Falls prevention exercise programs
• Viral diseases- poliomyelitis, AIDS
• Protease inhibitors- reduces the assembly of viral
particles and may reduce and possibly reverse the
neurological manifestations of AIDS

44. Infectious Diseases
• Antimicrobial therapy-side effects, allergies
and suppression of normal flora
• Therapists should ask clients to exercise under
conditions in which they may potentially have
a compromised immune response because of
trauma, pathological condition or surgery.
• As these conditions may make clients more
susceptible to infection, slow healing and slow
recovery.

45. Infectious Diseases
• Infection control in the rehabilitation environment is
essential to stop the spread of the disease.
• Therapist must be serious about the infection control
procedures while treating these patients-
handwashing, updating vaccinations, and cleaning all
the equipment.
• Educating clients to use antibiotics only when
needed(antibiotic-resistant bacteria due to overuse of
antimicrobial drugs) and complete the entire course of
medication can potentially slow the proliferation.

46. Infectious Diseases
• Adverse effects of antimicrobial and antiviral
drugs- nephrotoxicity and ototoxicity
(aminoglycosides), vertigo (tetracyclines),
neurotoxicity (metronidazole)- therapist must
be aware of adverse side effects to assist with
early recognition and referral to physician

47. Stroke, Hypertension and Related
Disorders
• Stroke- interference with the blood flow and
oxygenation produces both reversible and
irreversible neurological deficits
• Loss of function- two major causes
1. Loss of oxygenation to brain region. Followed by
glutaminergic rebound and excessive calcium
influx with apoptosis (programmed cell death)
• Drugs are aimed at restoring blood flow and
inhibiting glutaminergic hyper-excitability and
intracellular apoptotic mechanisms.

48. Stroke, Hypertension and Related
Disorders
2. Reperfusion injury associated with oxygen radicals and
associated cellular damage.
• To reduce the damage associated with
thromboembolism, tissue plasminogen activator are
recommended- most effective when given within an
hour after vascular insult
• Beta-adrenergic antagonists- reduces heart rate
correspondingly reduce exercise tolerance
• CCB, alpha-adrenergic blockers- weakness, dizziness,
syncope, and cognitive disorders.
• Diuretics, ACE-inhibitors- changes in serum electrolyte
levels, affects the heart, vasculature, skeletal muscle-
causes impairments in the strength of contraction.

49. Stroke, Hypertension and Related
Disorders
• Abrupt discontinuation of antihypertensives
may result in hypertensive crisis- increasing
the risk of stroke and related disorders.
• Complications after stroke- UTI’s, MSK pain,
DVT, pressure sores, shoulder subluxation and
depression- health care providers must be
aware of adverse effects and any alteration in
function of heart that may occur in relation to
exercise.

50. Stroke, Hypertension and Related
Disorders
• Anticoagulants- heparin, warfarin, aspirin (blood
thinners)- bleeding, allergic reactions,
thrombocytopenia, stomach irritation, more
susceptible to bruising- thus therapist must take care in
client handling and choice of activity.
• Antiarrhythmic drugs-used to restore normal
conduction patterns of heart-SE lightheadedness,
orthostatic hypotension, low blood sugar levels or
change in thermoregulation
• Therapists must be aware and prepared for
hypotensive events and need to educate clients on
positions that will reduce the effects of orthostatic
hypotension.

51. Stroke, Hypertension and Related
Disorders
• Antihypertensive medications are used to lower
blood pressure by limiting plasma volume
expansion, decreasing peripheral resistance and
decreasing plasma volume
• SE- increased urinary frequency, fatigue,
dizziness, orthostatic hypotension, tiredness, cold
hands and feet.
• People on antihypertensive medications require
careful cardiovascular monitoring, perceived
exertion during any physical activity

52. Pulmonary Diseases
• Many clients with neurological problems have
pulmonary diseases as well.
• Adrenergic bronchodilators- albuterol
epinephrine, metaproterenol, increases heart
rate and tremor- these drugs may exaggerate the
motor impairments.
• Theophylline in asthma and COPD can produce
changes in cognitive function including delusions,
hallucinations, tremor and nausea with higher
doses

53. Pulmonary Diseases
• Leukotriene modifiers (montelukast,
zafirlukast)- for management of asthma also
neurological and cardiovascular side effects of
these drugs are reduced when compared to
other agents.
• Lack of compliance with these medications
decrease pulmonary gas exchange ultimately
decreasing motor performance

54. Pulmonary Diseases
• Clients may have signs and symptoms of lung
dysfunction during exercise including
nonproductive cough, dyspnea, alterations in
breathing rate and chest expansion, changes in
skin color, as well as changes in auscultation and
percussion findings.
• Symptomatic pharmacotherapy may be required
to reduce disease-related symptoms such as
shortness of breath and improve exercise
tolerance
• Client should begin exercise after medications to
improve exercise tolerance

55. Pulmonary Diseases
• Oxygen therapy is indicated during exercise for
patients whose levels become desaturated
during low-level activity.
• Thus understanding the use of
pharmacological treatments for pulmonary
dysfunction can assist the rehab specialist in
promoting improved strength, exs tolerance,
functional abilities in clients with pulmonary
dysfunction.

56. References
• Umphred’s Neurological Rehabilitation; Sixth
Edition; Darcy A. Umphred, Rolando T. Lazaro,
Margaret L. Roller, gordon U. Burton.

57. • THANK YOU!