Brain region
Hemisphere
Functional region
Stroke symptom
Cortex
Left
Language
Speech fluency or language (Aphasia)
Vision
Visual field defects
Sensorimotor
Right-sided sensory impairment and/or hemiparesis or hemiplegia
Cognition
Inability to read and/or write
Right
Sensorimotor
Right-sided sensory impairment and/or hemiparesis or hemiplegia
Vision
Visual field defects
Higher sensory processing
Neglect of left side of body
Inability to recognize body parts and depth perceptual problems
Structures
Stroke symptoms
Subcortex
Internal capsule
Lacunar syndrome (Table 6.2)
Basal ganglia/thalamus
Lacunar syndrome (Table 6.2)
Brainstem
Cranial neuropathies and unilateral or bilateral weakness (e.g. locked-in syndrome)
Lacunar syndrome (Table 6.2)
Cerebellum
Headache
Vertigo
Nystagmus
Truncal or appendicular ataxia
Warning signs of stroke include sudden numbness or weakness on one side of the body or a limb, speech changes (i.e., dysarthria), language deficits (i.e., aphasia), sudden visual problems (i.e., diplopia, unilateral vision loss, or visual field defects), and sudden incoordination and gait difficulty.
Various brain regions are implicated based on the types of symptoms present. A change in the level of alertness accompanied by headache, nausea, or vomiting is highly suggestive of an intracerebral hemorrhage that can occur in the cortical regions, subcortical structures, such as the basal ganglia and thalamus, brainstem or cerebellum. Tables 6.1 and 6.2 contain detailed descriptions of specific localizing symptoms and stroke syndromes.
Table 6.2
Types of lacunar stroke syndromes
Lacunar syndrome | Clinical manifestations |
|---|---|
Pure motor hemiparesis | Unilateral motor weakness of the face, arm, and leg |
Pure hemisensory deficit | Unilateral numbness or paresthesia of face, arm and leg |
Mixed sensorimotor | Unilateral weakness and numbness in face, arm, and leg |
Dysarthria—clumsy hand | Unilateral lower facial weakness with slurred speech and impaired coordination with ipsilateral hand |
Ataxia—hemiparesis | Mild unilateral weakness in leg greater than arm with ipsilateral cerebellar signs that are out of proportion to the weakness |
What medications is the patient taking?
Important medications to query about include use of anticoagulants, antiplatelet agents, antihypertensives, opioids, antihyperglycemic drugs, and anticonvulsants.
6.3.1.2 Conducting a Home-Based Stroke Assessment [3, 4]
1.
Obtain vital signs (e.g., blood pressure, heart rate, temperature) and a bedside fingerstick glucose
2.
Perform a basic neurological exam
(a)
Evaluate patient’s orientation
(b)
Have patient repeat a sentence: “Today is a sunny day.”
(c)
Have patient follow three simple commands: Raise your right arm, stick out your tongue, show me two fingers with your left hand.
These tasks will enable the examiner to identify an aphasia or dysarthria. Common aphasias include the following:
Broca’s aphasia—speech is nonfluent with impaired repetition and preserved command-following.
Wernicke’s aphasia—speech is fluent, nonsensical with impaired repetition and command-following.
Conduction aphasia—speech is fluent with preserved command-following, but impaired repetition.
(d)
Have patient follow your finger with their eyes in all cardinal directions.
A gaze preference to one side, while at rest, suggests the presence of a visual field defect that is consistent with a hemispheric stroke. Patient’s eyes tend to look toward the side of the brain affected by the stroke. A centered gaze at rest with impaired eye movement(s) indicates a brainstem lesion.
(e)
Have patient close their eyes tightly and smile
Check for eye closure weakness by gently pulling up on their upper eye lids against resistance. Carefully observe their lower face for an uneven smile. A stroke affecting the motor system produces lower facial asymmetry and the presence of both eye closure and lower face weakness with the absence of limb weakness is likely a Bell’s palsy.
(f)
Have patient raise both arms in front of them and count to 10. Have them do the same for each leg separately. Drifting downward or difficulty elevating the limb confirms weakness.
(g)
Test tactile sensation by using a cotton swab or pinprick on both sides of the face, arms, and legs with patient’s eyes closed.
Afterward, simultaneously test sensation on both arms and legs to determine whether patient is demonstrating extinction to one side. Neglect or inattention of the left hemibody is a higher sensory modality related to right cerebral cortex impairment.
(h)
Conduct finger–nose–finger and heel–shin tests on both sides to determine the presence of limb ataxia. Overshooting or past-pointing and clumsiness during these tests suggest cerebellar involvement. It should be noted that marked weakness or confusion may limit the findings on this test.
6.3.1.3 What Is a Transient Ischemic Attack?
A transient ischemic attack (TIA) is a reversible focal neurological deficits occurring in any cerebral vascular territory that last less than 1 h and completely resolve in 24 h with no objective neurological findings.
6.3.2 Advanced Directives and Stroke Management
Based on a patient’s care preferences and or advance directives, expedited transfer to an acute care center would be warranted in those eligible for TPA or in a stupor or coma. Studies have shown that stroke patients who receive TPA have a greater chance of returning home as opposed to requiring high-level nursing home care.
If a patient’s preferences discourage hospitalization, a palliative and home stroke care support approach should be instituted based on the wishes of the patient and family members.
6.3.2.1 Strategies for Home-Based Management of Acute Stroke
1.
Elevated blood pressure (BP) in the setting of a stroke is a compensatory mechanism to maintain cerebral perfusion. Rapid reduction can worsen the patient’s symptoms. Systolic BP >185 and <220 is usually permissible for the first 48 h of a stroke, before it can slowly be reduced. Hypotension is unusual during an acute stroke and other etiologies for patient’s symptoms should be explored. SBP should be maintained closer to 140–160 if an ICH has occurred or there is suspicion for it.
2.
Check fingerstick glucose as hypoglycemia or hyperglycemia are stroke mimics and are reversible following rapid glucose correction.
3.
Obtain electrolytes, a complete blood count, and PT/PTT to evaluate renal and liver function, coagulopathies, and blood dyscracias.
4.
Obtain ECG if atrial fibrillation or other arrhythmias are suspected. Anticoagulation therapy is recommended in cases where cardiac arrhythmia is found (e.g., persistent or paroxysmal atrial fibrillation). Start an antiplatelet agent on the first day, if the stroke is deemed to be ischemic.
Initial Therapy Alternatives
Aspirin (81–325 mg) daily
Aspirin 25 mg/extended release dipyridamole 200 mg daily
Clopidogrel 75 mg (preferable for patients with an aspirin allergy) daily
5.
Check swallowing function by having patient drink 3–5 ml of water. The presence of coughing or a “wet” voice may warrant placing patient on an NPO status to reduce their aspiration risk until a formal home-based swallow evaluation is done by speech therapy, depending on the patient’s goals of care and the extent of the stroke. Some patients with dysphagic stroke can recover swallowing function over several weeks, so may benefit from hospitalization for temporary placement of a percutaneous feeding tube. Hydration support will be important in these cases as well until nutrition status is established. If home-based clinicians lack staffing and equipment for home IV fluids, urgent transfer to a higher level of care should be considered. Patients who are obtunded or in a stupor may require a nasogastric tube to be placed for nutrition and medications unless otherwise stipulated by advanced directives or their health care proxy.
6.
Comfort measures should be enacted immediately if a patient shows signs of cerebral herniation (e.g., irregular breathing, decerebrate or decorticate posturing, downward gaze deviation).
6.3.2.2 Home-Based Management of TIA [5]
If a patient’s neurological deficit is not resolving within 1 h or has not completely resolved over 24 h, it is recommended to send the patient to the emergency department for evaluation or manage his/her condition as an acute stroke in the home setting.
Complete resolution of the neurologic deficit necessitates determining patient’s stroke risk factors. The ABCD2 score [6], which takes into account age, blood pressure, and clinical symptoms, can be used to risk stratify TIA patients for the likelihood of having a stroke.
Risk Stratify Based on ABCD2 Score
Age ≥60 (1) point
BP >140/90 (1) point
Clinical symptoms with focal weakness (2) points
Speech impairment w/o weakness (1) point
Duration ≥ 60 min (2) points or 10–59 min (1) point
Scores greater than 6 suggest a greater than 10 % stroke risk within 1 week and closer to 20 % chance in 90 days. Therefore, patients suspected of having a TIA should be screened for obesity, hypertension, diabetes, hyperlipidemia and managed aggressively. Based on a patient’s goals of care and projected life expectancy, a pragmatic approach to managing the following risk factors should be employed to sustain an optimal quality of life:
1.
Begin treatment with an antiplatelet agent, either aspirin (81–325 mg), aspirin 25 mg/extended release dipyridamole 200 mg, or clopidogrel (75 mg)
2.
Aim for BP <140/90, which can be lowered with antihypertensive agents within 24 h.
3.
Aim for glycemic control—AIC <7.0
4.
Aim for total cholesterol <200, LDL <100,
5.
Aim for BMI <25; obese patients should also be considered for evaluation of the presence of sleep apnea as it can increase the risk of cardiovascular disease and stroke.
Though no one risk factor(s) is greater than another, ensuring that hypertension and glycemic control are achieved can minimize complications from an acute stroke while directly reducing risk of an intracerebral hemorrhage and hyperglycemic/hypoglycemic induced stroke-like symptoms.
6.3.2.3 Management of Homebound Chronic Stroke Patients
Determine patient’s level of disability and tailor therapy based on residual symptoms. Physical, occupational, and speech therapists are often required for management and retraining of limb movements, gait, cognitive, and speech/language deficits. Such therapy in an enriched interactive environment reduces overall disability and provides opportunity for stroke patients to regain a level of independence. Worsening of chronic stroke symptoms should prompt an evaluation for infectious, metabolic, or epileptic causes by the home-based provider.
Management of Spasticity: (See Spasticity section in Spinal Cord Injury)
6.4 Movement Disorders
6.4.1 Parkinsonism
The cardinal symptoms of Parkinsonism are a constellation of bradykinesia along with muscle rigidity, tremor, and postural instability.
Bradykinesia is most important for the diagnosis and is characterized as a decrease of rapid sequential movement on examination with lack of spontaneous, automatic movements. Its clinical manifestations include small handwriting that tends to trail off (micrographia), reduced facial expression (masked facies), and/or reduction in vocal intonation (hypophonia).
Rigidity, or muscle stiffness, is related to increased muscle resistance during passive limb movement that produces a ratcheting feeling similar to a “cogwheel.” Very mild rigidity usually requires coactivation maneuvers of the contralateral limb in order to elicit it.
Parkinsonian tremor is primarily present at rest involving the fingers, usually the thumb and index, to produce the characteristic pill-rolling tremor. Tremor abates during action and tends to re-emerge after a brief delay.
Postural and gait changes in parkinsonism are characterized by a stooped posture, reduced stride length producing a shuffling appearance to the gait, and multi-pivot turning. In addition, impairment or loss of postural reflexes places many of these patients at risk of falling. A pull test, in which the examiner stands behind the patient and pulls them backwards while monitoring the number of steps they need to recover without assistance is often utilized. Greater than 2 steps to recover or the need of the examiner to prevent them from falling is abnormal.
Furthermore, these patients can develop gait freezing, whereby they stutter step in place or one or both feet suddenly seemed pasted to the floor when walking normally or through small spaces such as doorways, turning, and/or upon initiating walking. Failure to compensate by holding on to someone or an assistive device increases the risk of falling. This can be seen late in the disease course for Parkinson’s disease (PD), but rather early on among the atypical parkinsonism syndromes.
6.4.1.1 Classification and Treatment of Parkinsonism
Parkinson’s Disease
Parkinsonism results from either a degenerative disease or an acquired etiology (e.g., medications, toxins, infections, vascular). Among the degenerative causes, Parkinson’s disease is the most common and an accurate diagnosis is predicated upon a clinical assessment, which clinic-pathological studies [7] have shown to have a greater than 90 % accuracy. This is based on the presence of an asymmetric bradykinesia with at least 1 concomitant symptom: muscle rigidity, tremor, and/or postural and gait instability. Further supportive features include a slow progression with sustained, robust levodopa response.
Distinguishing PD from atypical parkinsonism has both treatment and prognostic implications, as the latter conditions do not respond well to levodopa, and have a more rapid and deleterious clinical course. The atypical parkinsonism syndromes include progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), multisystem atrophy (MSA), and dementia with Lewy Body (DLB) [8].
6.4.1.2 Treatment of Parkinson’s Disease
The treatments for PD are symptomatic with levodopa being the gold standard. It is reasonable to start symptomatic treatment in the early stages of the disease when the level of severity is starting to adversely impact quality of life and daily activities. See Table 6.3.
Table 6.3
Pharmacological treatment for Parkinson’s disease
Medication class | Formulations | Initial doses | Clinical considerations |
|---|---|---|---|
Levodopa | Carbidopa/levodopa, Carbidopa/levodopa ODT | Start 25/100 mg three times per day | Nausea |
Lightheadedness | |||
Hallucinations | |||
Dopamine agonists | Pramipexole | Start 0.25 mg three times daily, max 4.5 mg daily | Impulse control disorders |
Hypersomnolence | |||
Cognitive deficits | |||
Hallucinations | |||
Pramipexole extended release | Start 0.375 daily, max 4.5 mg daily | ||
Ropinerole | Start 0.25 mg three times daily, max 24 mg daily | ||
Ropinerole extended release | Start 2 mg daily, max 12 mg twice daily | ||
Rotigotine TD | Start 2 mg daily, max 16 mg/24 h | ||
MAO-B inhibitors | Selegiline | 5 mg twice daily | Dizziness, headache, dyspepsia |
Rasagaline | 1 mg daily |
Motor Symptom Management
Levodopa is considered the first line therapy in patients older than 70 years. Providers should initiate levodopa in immediate-release formulations with a titration to at least three times per day. Nausea related to levodopa can be treated with extra carbidopa or domperidone taken with each dose of levodopa. Should patients develop levodopa-induced hallucinations or psychosis, incorporating quetiapine or clozapine into the regimen is often efficacious.
The dopamine agonist class or monamine oxidase (MAOB) inhibitors can be utilized early on in patients less than 70 years who are cognitively intact. Short-acting dopamine agonists are administered three times per day. Long-acting formulations exist for both pramipexole and ropinerole and can be used once a day, but oftentimes are dosed two to three times daily The rotigotine patch is utilized daily and should be changed and applied on different body regions (e.g., upper limbs, torso, back) at the same time each day to ensure continuous benefit. There are no clinical data demonstrating superiority of one agonist over another. Dopamine agonists can cause excessive sedation, sleep attacks, hallucinations, and impulse control disorders (e.g., gambling, hypersexuality, shopping). It is important to screen patients for these potential side effects, as reduction in dose or discontinuation the medication is ameliorative.
Patients on longstanding levodopa therapy can develop “wearing-off” episodes also known as motor fluctuations. As the disease progresses, the hours of good motor response (“on” time) per dosing interval decrease, while precipitous “off” periods increase. This along with the emergence of dyskinesia, involuntary muscle movement flowing from one region of the body to another, reduces a patient’s quality of life.
Dystonia is involuntary contraction of muscle groups that cause abnormal twisting or repetitive movements or postures. Common focal dystonias that can develop in PD include the following.
Cervical dystonia
Blepharospasm (involuntary eyelid closure or spasms) or eyelid opening apraxia
Hand dystonia
Lower limb dystonia (e.g., toe curling or foot dystonia)
Camptocormia (abnormal anteroflexion of the trunk)
Pisa syndrome (lateral flexion of the trunk)
In order to manage motor fluctuations, dyskinesia, and other involuntary movements such as dystonia, it is important to initiate discussions with a neurologist who is willing to offer management guidance, even if the patient is unable to come in to a neurology office visit. The pharmacological strategies that are oftentimes considered are listed in Table 6.4.
Table 6.4
Management approaches for motor complications and dystonia in Parkinson’s disease
Motor fluctuations/wearing “Off” | Increase levodopa dose and/or dosing frequency |
Add COMT-I | |
Add MAOBI | |
Switch levodopa formulation to carbidopa levodopa extended release capsules (Rytary) | |
Add a dopamine agonist | |
Utilize apomorphine SC injections | |
Dyskinesia | Reduce dose or frequency of levodopa |
Discontinue COMTI | |
Discontinue MAOBI | |
Add amantadine 100 mg three to four times daily | |
Focal dystonia | |
Cervical Blepharospasm/eye-lid opening apraxia Hand dystonia Camptocormia Lower limb Pisa syndrome | Baclofen (Start 5 mg three times daily, max 80 mg daily divided) |
Low dose benzodiazepines (clonazepam, diazepam, lorazepam) dosed two to three times daily | |
Trihexyphenidyl (2 mg twice to thrice times daily, max 12–15 mg daily divided) | |
Botulinum toxin injections |
There is little to no superiority data for the different classes of antidystonic agents. Uses of these therapies are based on the patient’s tolerance and the existence of other underlying medical comorbidities. Botulinum toxin injections have emerged as the first line treatment choice for many of the focal dystonias, due to its targeted clinical efficacy and minimal risk of constitutional and cognitive adverse effects.
Surgical Strategies
As the disease progresses, pharmacological permutations not only become more complex, but the propensity for side effects increases.
Deep Brain Stimulation
Deep brain stimulation (DBS) is an effective treatment for the management of the cardinal Parkinson’s motor symptoms, including refractory tremor. It should be considered in patients who have idiopathic PD and not atypical variants, demonstrate robust levodopa response, lack dementia or signs of atypical parkinsonism, and have motor complications (e.g., motor fluctuations, dyskinesia) requiring higher dopaminergic dosages.
Compared to best medical therapy, DBS produces longer “on” time for patients with dramatic reductions in wearing offs, dyskinesia, and medication burden. It can also benefit focal dystonia that emerge as a consequence of disease progression or levodopa complication.
Carbidopa/Levodopa Intestinal Gel
This specially formulated enteral gel is particularly useful for a patient with advanced PD with motor complications, who also has cognitive dysfunction and/or dysphagia that affects oral intake. It significantly increases “on” time while reducing dyskinesia by continuously infusing carbidopa/levodopa through a gastrostomy–jejunostomy tube (PEG-J) 16 h per day.
6.4.1.3 Nonmotor Symptom Management (Refer to Table 6.5)
Table 6.5
Nonmotor symptom management in Parkinsons’ disease
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