Transcript Neurology Case presentation

Kimberly Johnson, MD, PGY-2
HPI
 53 y/o gentleman who presented to the ED with
dizziness and was found to have blood pressure of
297/132. He was admitted for hypertensive crisis and
started on a nitro drip and later switched to a cardene
drip.
 On HD #1, patient woke with trouble swallowing,
feeling dizzy when sitting up and having double vision
that improved when he closed one eye
 On assessment patient was thought to have possible
left eye lid droop. Neurology was stat consulted.
Cont HPI
 PMH: Smoking for 25 years ( 1.5 ppd)
 MEDS: On admission no medications.
 On transfer to neurology: amlodipine and aspirin,
lovenox,
 Family history: DM, Hypertension
 Social history: Worked in construction
Physical Exam
 General: Well nourished obese gentleman in no acute
distress
 HEENT: NCAT, Nares Patent, Trachea midline
 Cardiac: RRR, no murmurs heard
 Resp: CTA bilaterly
Neurological Exam
 Mental Status: Awake, alert, oriented x4
 Speech: Able to name, repeat, comprehend, with moderate dysarthria
 Cranial Nerves: Significant for right sided miosis, left side equally
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reactive to light, EOMI, visual field/acuity normal. Decreased temp
sensation on right side of face. TRAP/SCM strength 5/5, palate raises
symmetrically, tongue midline.
Motor Strength: Normal bulk and tone with 5/5 strength throughout in
upper and lower extremities.
DTRs: 2+ in bicep, tricep,brachielradialis,patellar, 1+ in ankles, toes
downgoing bilaterally
Sensation: Normal light touch throughout, decreased temperature on
left arm
Coordination: Finger to nose intact, heel to shin slow, but intact
Gait: Feeling unsteady, leaning to the right, able to ambulate with
walker
Where
What
MRI findings
Wallenberg Syndrome
• First described in Dr. Vieusseux in 1808, then by Dr. Adolf
Wallenberg in 1895 clinically and 1901 by autopsy.
• Caused by occlusion of the posterior inferior cerebellar
artery or a branch off the vertebral artery
• Most commonly affected arteries in order are Vertebral,
PICA, Superior middle and inferior medullary artery.
•This is the most common Posterior circulation infarct
Lateral medullary syndrome
(location) symptoms
Vestibular Nuclei
Vomiting, vertigo, nystagmus
Inferior cerebellar peduncle
Ipsilateral ataxia, dysmetria past
pointing
Central tegmental tract
Palatal myoclonus
Lateral Spinothalamic tract
Contralateral deficits in pain and
temperature sensation, limbs and
torso
Spinal trigeminal nucleus
Ipsilateral loss of pain and temp in
face
Nucleus ambiguus
Ipsilateral laryngeal, pharyngeal,
palatal hemiparalysis, dyphagia,
diminished gag reflex
Descending sympathetic fibers
Ipisilateral Horner’s syndrome
(ptosis, miosis, and anhydrosis)
Lateral medullary syndrome
(location) symptoms
Vestibular Nuclei
Vomiting, vertigo, nystagmus
Inferior cerebellar peduncle
Ipsilateral ataxia, dysmetria past
pointing
Central tegmental tract
Palatal myoclonus
Lateral Spinothalamic tract
Contralateral deficits in pain and
temperature sensation, limbs and
torso
Spinal trigeminal nucleus
Ipsilateral loss of pain and temp in
face
Nucleus ambiguus
Ipsilateral laryngeal, pharyngeal,
palatal hemiparalysis, dyphagia,
diminished gag reflex
Descending sympathetic fibers
Ipisilateral Horner’s syndrome
(ptosis, miosis, and anhydrosis)
Nucleus ambiguus
 The nucleus ambiguus (literally "ambiguous nucleus")
 Located dorsal (posterior ) to inferior olivary nucleus
in the lateral portion of upper medulla.
 Recieves UMN innervation directly via corticobulbar
tract.
 Nucleus gives rise to branchial efferent fibers of Vagus
N, (Innervating laryngeal, pharyngeal and uvulae
muscles)
 Also efferent motor fibers of Glossopharyngeal N.
(Innervating stylopharyngeus muscle) and Accessory
N (Laryngeal muscles as well)
Wallenberg Syndrome and
Dysphagia
 Dysphagia is a disorder of deglutition.
 Affects Oral, Pharyngeal, and/or Esophageal phases of
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swallowing.
Estimates of the incidence vary widely from 29% to 81%
Specifically for Lateral Medullary infarcts vary from 55 % 100%
Aspiration was found to range from 22 – 55%, with nearly
half of these being silent aspirations.
Nutritional needs post stroke have been shown to have
significant affects on recovery.
Table 1: Micronutrients and mechanisms through which
their deficiencies induce cerebrovascular alterations and
increase the risk of stroke.
Back to our patient’s dysphagia
 Patient had Video Swallow on 3/23/12
 Oral Stage Summary*: Patient had significant difficulty with PO intake, coughing,
and poor management of secretions.
 Pharyngeal Stage Summary*: Pharyngeal stage characterized by delayed swallow
initiation with the bolus head in the pyriforms for tsp of nectar thick liquid. Overall
movements of the swallow were considered inconsistent which may be due to
etiology of the stroke (brain stem) but also due to frequent movement, coughing,
expectoration due to reduced management of secretions.
 Prognosis*: Fair
 Dysphagia Rating*: Moderately-Severe Dysphagia -Not able to swallow safely by
mouth for nutrition/hydration but may take some consistency w/ consistent max
cues in therapy only. Alternative method of feeding required.
 Penetration Aspiration Scale*: Material enters laryngeal vestibule, passes
below vocal folds & no effort is made to eject
 PEG tube placed on HOD #7. Continued Speech therapy.
Our patient’s story continued.
 Repeat swallow study on Post stroke day 15 patient was
able to take Mechanical soft, with nectar thickened
liquids.
 Taking in <50% of calories to maintain adequate
nutrition.
 Patient discharged home with PEG tube in place, with
plan for removal 2 weeks after discharge.
 Patient will Outpatient Speech therapy but was
uninsured and has not been seen yet in follow up.
Conclusion
 Dysphagia is a common consequence of lateral
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medullary infarcts.
Consequence of dysphagia is aspiration, with 50%
being silent, with patient’s facing the complication of
aspiration pneumonia
PEG tube placement vs NG tubes
Patient’s will regain their ability to be able to have oral
nutrition adequate for their needs
Understanding malnutrtion and its role in stroke
recovery is critical in our patients returning to their
pre-stroke quality of life.
References
 Bath PMW, Bath-Hextall FJ, Smithard D. Interventions for dysphagia in
acute stroke (Review). The Cochrane Library 2009, Vol. 1
 M Dennis, S Lewis, G Cranswick and J Forbes, on behalf of the FOOD Trial
Collaboration. FOOD: a multicentre randomised trial evaluating feeding
policies in patients admitted to hospital with a recent stroke. Health
Technology Assessment 2006; Vol. 10: No. 2
 ANTHONY J, KAPIL K, A. BARNEY H. Long-term outcome of percutaneous
endoscopic gastrostomy feeding in patients with dysphagic stroke. Age
and Ageing 1998; 27: 671 -676
 Bouziana SD Tziomalos K. Malnutrition in Patients with Acute Stroke. Journal
of Nutrition and Metabolism Volume 2011, Article ID 167898, 7 pages
 Marik PE and Kaplan D. Aspiration Pneumonia and Dysphagia in the
Elderly*, Chest 2003;124;328-336
 Gloss D, Weisberg L. Neurlogy for the Specialty Boards, 2007, 1st Edition
 http://www.neuroanatomy.wisc.edu/virtualbrain/BrainStem/09NA.html
Frequency of Vascular Occlusive
lesions in a registry of posterior
circulation infarcts
Artery
Frequency
Innominate artery
0.7% (2)
Subclavian artery
1.9% (5)
ECVA
43.5% (113)
ICVA
41.5% (108)
Basilar artery
41.8% (109)
PCA
15% (39)
Includes only lesions of the first portion of the ECVA. Distal ECVA
dissections were not included.
Transverse section of the upper
medulla