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Neurology and nutritionNeurology and nutrition
Dr Anhar Hassan, Dr Brendon Boot
Senior Neurology Registrar
Royal North Shore Hospital
ObjectivesObjectives
be able to describe the neurological disorders which give rise to dysphagia
be able to describe the assessment of dysphagia be able to describe nutritionally relevant stroke risk factors provide or use in the presentation medical terminology and
abbreviations for these disorders biomedical parameters and diagnostic tests and how these
change with disease progression or improvement medications and other treatments associated with the
management of the neurological disorders discussed
Neurological disorders Neurological disorders resulting in dysphagiaresulting in dysphagia
Neurology deals with many conditions, affecting the peripheral or central nervous system:
Acute, may improve– Stroke
Acute on chronic– Multiple sclerosis
Progressive– Motor neurone disease– Parkinsons disease– Huntington’s disease
Case 1: Mrs J.V.Case 1: Mrs J.V.
72 yo lady 2 years progressive weakness initially of upper then
lower limbs, later bulbar and respiratory muscles. Diagnosed with motor neurone disease- no
treatment to significantly alter disease progression Progressive difficulty walking- now transfers only
to and from wheelchair with assistance of her husband. Needs assistance of husband for all activities of daily living
Case 1: Mrs JVCase 1: Mrs JV
Noticed soft speech Difficulty swallowing, ineffective cough triggered
by food and long periods of time taken for small meals. Drooling a major inconvenience and some “choking” episodes (unpredictable)
Marked weight loss- 45 kg at presentation, 5-6 kg loss in the 3 weeks prior to presentation after no oral intake
Presented with breathlessness and clinically dehydrated, malnourished and in respiratory failure
Mrs JV managementMrs JV management
Speech therapist assessment - safe for thickened fluid and puree diet, dietitian calculated that her intake would not equal her nutritional requirements
Hydrated, receiving all nutritional requirements through percutaneous endoscopic gastrostomy (PEG) feeding tube
Discharged with noninvasive ventilator with the aim to use it at night when most desaturations occur and anytime when breathless
Discussed end of life decisions again- particularly if unwell Linked in to community palliative care service and motor
neurone clinic follow up service
Motor neurone diseaseMotor neurone disease
Degeneration of both upper and lower motor neurones Weakness often asymmetric in legs, hands, proximal arms or
oropharynx. No sensory impairment. Usually mentally alert. Respiration is usually affected late.
Weight loss occurs from a combination of wasting and dysphagia. Cranial nerve nuclei affected: dysarthria, lingual wasting and
fasciculation and impaired movement of the tongue. Dysarthria and dysphagia is caused by upper motor neurone
disease (pseudobulbar palsy). The uvula does not move well (or at all) on phonation but a vigorous response is seen in the pharyngeal or gag reflex.
MND managementMND management
1. Nutrition2. Ventilation and protect against aspiration3. Nursing care 4. Medications: No cure
– Riluzole (glutamate inhibitor)- prolongs life by 3 to 6 months with no improvement in function or quality of life
– Botulinum toxin injections to treat siallorrhea
MND multi-disciplinary clinicMND multi-disciplinary clinic
Assessed as a day stay patient by all members of the team and then follow up arranged in the outpatient clinic via a nursing coordinator
Team members:– Neurologist– Respiratory physician– Respiratory clinical nursing consultant– Physiotherapist– Occupational therapist– Speech therapist – Dietitian– Social worker
MND prognosisMND prognosis
Mean duration of symptoms is 4 years. – Bulbar onset MND is slower to progress
Death is usually from respiratory failure, aspiration pneumonia or pulmonary embolism after prolonged immobility.
Case 2: Mrs SCCase 2: Mrs SC
82 year old ladyLives alone following the admission of her
husband to a nursing home after his stroke. Supported by a friend.
A slowly progressive dementia has been noticed by her friend (aware of people but often forgets recent events)
Mrs SC presentationMrs SC presentation
Sudden onset: Hemiparesis (unable to move right side) Global dysphasia- follows 1 step commands
unreliably and has fluent but nonsensical speech (conversational “niceties” are reasonably preserved)
Noted to be in rapid atrial fibrillation with a small acute myocardial infarction noted on tests.
MRI: MRI: DWI- L middle cerebral artery territory strokeDWI- L middle cerebral artery territory stroke
Mrs SC: progressMrs SC: progress
Aspiration pneumonia noted on day 3 of admission. When first reviewed on arrival (Saturday morning) in emergency she had been “trialled” on a puree diet in the absence of speech therapists to formally assess her till Monday. Food was pooling in her mouth which she seemed unaware of.
Cardiac failure ensued with recurrent runs of rapid atrial fibrillation. Medical management was limited by hypotension.
Mrs SC: management issuesMrs SC: management issues
Immediately life threatening– Rapid atrial fibrillation due to hemodynamic compromise
and risk of further heart attack.– Heart failure– Aspiration pneumonia
Nutrition– Able to have grade 2 thickened fluids. – With the major fluctuations in her other comorbidities,
she was not receiving adequate nutrition so additional nasogastric tube feedings were considered.
Mrs SC: management issuesMrs SC: management issues
Preventing further strokes (secondary prevention)– Likely embolic: Anticoagulation (presumed clot from the
fibrillating heart)– Exclude other causes (carotid artery disease)– Manage stroke risk factors
Functional status after this stroke– Unable to “learn” due to dementia and aphasia.
Rehabilitation is not possible. Due to ongoing severe weakness and dependence, she requires nursing home care.
– Friend applied for guardianship to organise her affairs
StrokeStroke
Two types:
1. Infarction (interrupted blood supply) from emboli, unstable atherosclerotic plaques or small vessel disease
2. Haemorrhage secondary to artery weakness (amyloid in elderly, aneurysms etc) and hypertension
StrokeStroke
Presents with sudden neurological deficit. The distribution of weakness, sensory loss, visual or speech impairment, or neglect depend on the vascular territory involved. Unilateral weakness is characteristic of many syndromes.– eg, Middle cerebral artery territory which affects
face>arm>leg weakness to varying degrees and speech if the dominant (usually left) hemisphere is involved
Stroke prognosisStroke prognosis
Death ranges from 8-20% in first 30 days (higher for haemorrhages)
Death is mainly from cardiac (AMI, arrhythmias) or respiratory (aspiration pneumonia, pulmonary embolism) sources. Less deaths are due to brain swelling with herniation.
Dysphagia in strokeDysphagia in stroke
27-50% of stroke patients have dysphagia 50% of these die or recover spontaneouslyDysphagia causes increase risk of chest
infections, malnutrition, increased length of hospital stay and readmission to hospital.
Medical screening for dysphagia: sip testMedical screening for dysphagia: sip test
If constantly alert, position patient in upright position
Give 50 ML water in 5 ml stepsListen to patient’s voice and watch for
cough between sips– If coping with above, may have thin fluids and
appropriate diet– If drowsy or if signs of aspiration, patient
“fails” and has formal speech path review of swallowing
Dysphagia in strokeDysphagia in stroke
Nasogastric tube feeding - easy, quick, relatively noninvasive and safe.
Patients can pull them out; nasal ulceration limits duration.
PEG - invasive procedure (complications peritonitis, bleeding, perforation of abdominal organs). In the long term, they are more comfortable.
FOOD trialsFOOD trials
Underweight patients had increased mortality (OR for undernourished compared with normal, 1.82; 95% CI, 1.34 to 2.47)
Adding oral protein-energy supplements to standard hospital diet was not powered to show a significant benefit
Early (<1 week) versus late (>1 week) enteral feeding resulted in an absolute reduction in mortality of 5.8% (95% CI 0.8-12.5, p=0.09)
PEG feeding was associated with increased mortality and poor outcome (p=0.05)
Nutritionally relevant stroke risk factorsNutritionally relevant stroke risk factors
Hypertension– Low salt– Usually requires antihypertensive medication
Cholesterol– Measure total chol, HDL (good), LDL (bad),
triglycerides – Dietitian consult– In vascular patients, unless contraindicated, we start a
statin to lower cholesterol
Nutritionally relevant stroke risk factorsNutritionally relevant stroke risk factors
Diabetes: – Diagnosis
Fasting BSL <5.5 mmol/L- no further action required Fasting BSL 5.5-6.9- OGTT required Fasting BSL >7 mmol/L- repeat fasting BSL to confirm
– Management Refer to dietitian for diabetic diet, diabetic education unit
and endocrine team (may need oral hypoglycemic)
Case 3: Ms LPCase 3: Ms LP
38 yo lady Presented 9 years ago with R visual disturbance
– Delayed R visual evoked response– Dx: optic neuritis
9 months later, had clumsiness of her left limbs– Left cerebellar incoordination noted– Given pulse methylprednisolone (1g 3 days)
Diagnosed with multiple sclerosis after MRI, lumbar puncture and visual evoked responses.
Ms LP: current issuesMs LP: current issues
Subjective breathlessness and neuropathic pain limiting oral intake- presented dehydrated with marked weight loss
No objective change in weakness, clumsiness or sensory impairment of her cranial nerves or limbs.
Ms LP: Ms LP:
Strained voice (combined pseudobulbar and cerebellar dysarthria)
Marcus Gunn phenomenonmoderate asymmetric R>L limb clumsiness
with minimal pyramidal weakness, generalised brisk reflexes, independently mobile.
Ms LP: progressMs LP: progressGiven 3 days IV methylprednisolone
some improvement in the pain, but persistent subjective SOB.
Already on gabapentin Respiratory physicians investigating further
Commenced on beta interferon Aim to decrease frequency of relapses
Speech pathology, dietitian, physiotherapy, OT and social worker reviews.
Referred to rehabilitation
Ms LP: progressMs LP: progress
Infrequent relapses requiring infrequent steroids, no preventive treatment– Relapses too few to qualify for beta interferon
initiallySlow functional decline after each relapse
howeverStill living independently but too disabled
to work. (previous nanny)
Multiple sclerosis (MS)Multiple sclerosis (MS)
A chronic disease most commonly in young adults (peak incidence between 20-30 years old, females) with areas of inflammation and demyelination in the central nervous system.
Multiple sclerosis subtypesMultiple sclerosis subtypesTwo clinical pictures:
1. Relapsing remitting with secondary progressive MS- Usually starts as a relapsing remitting course of isolated exacerbations then turns into a chronic progressive, unremitting course. (80% of cases over 10-15 years)
2. Primary progressive MS- Symptoms include weakness, sensory disturbance, blurred vision due to optic neuritis, incoordination due to cerebellar involvement, bladder instability from spinal cord disease, and cognitive or personality change.
MS treatmentMS treatment Acute relapses are shortened by intravenous
methylprednisolone Recurrent relapses may qualify the patient for betaferon
therapy which has been shown to decrease relapses Side effects of medications commonly used include:
– Baclofen for spasticity- nausea, sedative– Oxybutinin for neurogenic bladder instability- dry mouth,
nausea, constipation, abdominal discomfort– Recurrent antibiotics for infections- nausea and diarrhea– Corticosteroids for relapses- osteoporosis– Interferons for prevention of relapses- “flu like symptoms”
including nausea, fatigue and depression
Dysphagia and nutrition in MSDysphagia and nutrition in MS Incidence of dysphagia reported from 3-43% in trials. Diet often limited by fatigue, reduced mobility, and other
disabilities affecting meal time efficiency (incoordination or visual impairment)
No relationship found between dysphagia and nutritional status in a group of 79 patients with a high incidence of dysphagia (43%).
No direct evidence but it is suggested to use dietary supplements (eg sustagen) as an effective means of improving the nutrient intake without impairing appetite for normal foods.
PEG feeding is an option also
Huntington disease: an example of a Huntington disease: an example of a neurodegenerative conditionneurodegenerative condition
Progressive hereditary disorder usually presenting in middle age.
Course of disease usually runs over a period of 15 years. More rapid in patients with earlier onset of age.
Characterised by:• Movement disorder (usually chorea)• Dementia• Personality disorder
Diagnosed by genetic testing No known treatment to alter the course of the disease. Treatment of depression and psychosis important
Parkinson disease (PD)- Parkinson disease (PD)- another neurodegenerative conditionanother neurodegenerative conditionOne of many causes of “parkinsonism”
(including drugs, other neurodegenerative processes, trauma, tumour, postencephalitic)
Degeneration of dopaminergic neurones in the basal ganglia
Mean age of onset 55 years Insidious onset, slow progression
PD: clinical featuresPD: clinical features Tremor at rest- “pill rolling” Rigidity Bradykinesia- slowed movements, small
handwriting, soft speech (hypophonia), loss of facial expressions (hypomimia) and dysarthria
Flexed posture and shuffling gait Poor balance and falls- loss of postural reflexes “Freezing” phenomenon Fluctuations increase with disease progression and
complexity of medical management- “on” vs “off”, dyskinesias usually peak dose
PD: managementPD: management No treatment has been proven to alter the underlying
neurodegenerative process but the mortality rate has dropped 50% since treatment with levodopa
Medications: Dopamine precursor (levodopa)- the most commonly used Dopamine agonists (bromocriptine) Dopamine releaser/glutamate antagonist (amantadine) Monoamine oxidase type B inhibitor (selegeline) Anticholinergics (benztropine)
Surgery: Ablation Deep brain stimulation
Neurology patients can be Neurology patients can be challenging…challenging…
Level of consciousness- variabilityPersonality or cognitive impairments-
compliance, information processingTreatments may interfere with nutrition-
drug side effects, ventilationDisability limiting access to best options Depression and fatigue are common-
undermine motivation
Important referencesImportant references Bath PMW et al. Interventions for dysphagia in acute
stroke (Cochrane review). The Cochrane library, Issue 1, 2002
FOOD Trial Collaboration. Poor nutritional status on admission predicts poor outcomes after stroke: observational data from the FOOD trial. Stroke. 34(6):1450-6, 2003 Jun
Donnan GA, Dewey HM. Stroke and nutrition: FOOD for thought. Lancet. Feb 2005; 365: 729-730.
Payne A. Nutrition and diet in the clinical management of multiple sclerosis. The British Dietetic Association 2001. J Hum Nutr Dietet. 14; 349-357.