Presentation on theme: "Points For Discussions Diagnosis. HISTORY 57 years old Malay lady underlying Mixed Mitral Valve Disease complicated with Atrial Flutter-Fibrillation not."— Presentation transcript:
HISTORY 57 years old Malay lady underlying Mixed Mitral Valve Disease complicated with Atrial Flutter-Fibrillation not on warfarin.
Admitted on 1 st July 2004 Complaint of : 1) Progressive lower limbs weakness x 3/7 prior to admission 2) Progressive inability to swallow x 3/7 prior to admission 3) Changes in voices following onset of inability to swallow 4)Dizziness instability
Further history: On 28 th June 2004 i.e; 3/7 prior to admission: 1) Patient started to have gradual onset of lower limbs weakness. She claimed that she felt weak to walk but still able to walk with assistance. The weakness become more prominence on the day of admission. It is confined to the left lower limb rather than the right lower limb. Later on she also noted that her left upper limb become weaker. It is associated with left sided numbness.
2) Patient also noted that she gradually feel difficulty to swallow on the same day of lower limbs weakness. She claimed that there is no difference in swallowing either fluid and solid food. The symptom become worse on the day of admission in which immediately after swallowing she experience nasal regurgitation. There was also episodes of choking.
3) Patient also claimed that she noted that her voices started to change since the onset of inability to swallow. She claimed that her speech sounds like nasal speech. 4) Complaining of dizziness (vertigo) on the day of onset of illness which persistence till today. It is associated with instability to walk. She claimed that she is afraid to walk due to feeling of tendency to fall if she walking.
Denied any preceding history of fever with headache or neck pain No history of loss of consciousness No history of similar episodes before No bowel or urinary incontinence No history of fever or URTI symptom Denied preceding history of palpitation or chest tightness
CLINICAL Comfortable,Conscious and alert GCS 15/15 BP: 139 /9 5 PR 102, AF Febrile : temperature 38.5 C on admission which settled after 3/7 of IV Cefuroxime and Metronidazole
Lungs: Clear CVS: S1S2 with loud S1 MDM and PSM at MA; Left parasternal heave Peripheral pulses irregularly irregular JVP not raised PA: soft and non-tender Funduscopy: no hemorrhage no papiloedema No neck stiffness
On day 1 of admission (1 st July 2004): T : 38.9 C Nystagmus positive Impaired past pointing No dysdiadokinesia Romberg’s sign positive- Fall to left side Right VII, IX, X, XII CN Palsy
Tone are all normal Power are all 4/5 except on Right upper limb Generalized hypereflexia Plantar is equivocal on left side and withdrawal on right side
On 2nd day of admission (2rd of July 2004) Temperature settling Right IX, X, XII CN palsy Jaw jerk normal No more past pointing No dysdiadokinesia
On 4 th day of admission (4 th July 2004) New neurological findings Left hemiparesis: power are 4/5 reflexes brisk plantar upgpoing Reduced sensation on left upper limb and lower limb
On day 5th and 6th of admission (5 th and 6th July 2004): GCS 15/15 No chyne stokes breathing Noted nasal speech Funduscopy: no papiloedema no hemorrhage Right eye ptosis Pupil 3 mm reactive to light and equal bilaterally
Fasciculation of tongue noted on right side Tongue deviated to the left Weakness of the right soft palate Gag reflex absent Cranial nerve XI intact No fatigability noted
No nystagmus No dysdiadokinesia No past pointing Romberg sign positive on Right Findings confined to left upper and lower limb Hypertonia on left Power are 4+/5 on left and 5/5 on right Reflexes are brisk on left Plantar up-going on left
On day 7th of admission (7th July 2004): GCS 15/15 No chyne stokes breathing Noted nasal speech Right eye ptosis Pupil on the right side is smaller than the left
No fasciculation of tongue noted Tongue slightly deviated to the left ( improved) Weakness of the right soft palate Gag reflex absent Other cranial nerve intact Proprioception intact
Romberg sign positive on Right Ataxia Findings confined to left upper and lower limb Hypertonia on left Power are 4+/5 on left and 5/5 on right Reflexes are brisk on left upper limb Areflexia both lower limb Plantar equivacle on left
12 lead ECG on 1 st July 2004; Atrial flutter- fibrillation CXR on 1 st July 2004: cardiomegaly with clear pulmonary fields Nerve conduction study on 7 th July 2004: normal ECHO on 8 th July 2004: Moderate MS, Trivial MR, dilated LA (4.13 cm) no intracardiac clots, no vegetation
CT scan of brain on 1 st July 20004 (day 3 of illness) reported as normal. MRI of brain on 7 th July 2004 (day 10 of illness) verbally reported as 1) Evidence of shower of emboli to both hemisphere predominantly on the right side; 2) Right parietal,Right centrum semi ovale 3) Small area in the right cererbellum 4) Right brainstem
MANAGEMENT IVI heparin started on 2 nd July 2004 adjusted according to APTT ratio. Heparin was off on 6 th July 2004. Oral Warfarin started on 2 nd July 2004; latest INR is 2.33 on 7 th July ( on Warfarin 3 mg od).
T Aspirin 150mg OD (started on 7 th July 2004) T Provastatin 20 mg oN T Stegeron 25 mg tds Oral Digoxin 0.25 mg od T Ranitidine 150 mg bd IV Cefuroxime 750 mg tds (started on 1 st July 2004) IV Metronidazole 500 mg tds (started on 1 st July 2004)
DISCUSSIONS Bulbar palsy results from bilateral impairment of function of the IXth, Xth and XIIth cranial nerves. This gives rise to dysarthria, dysphagia (often with choking episodes and nasal regurgitation of fluids), dysphonia and poor cough, and susceptibility to aspiration pneumonia.
The lowermost part of VII may, infrequently, be involved. The disturbance is of the motor nuclei rather than of the corticobulbar tracts. It is distinguished from pseudobulbar palsy by the presence of lower motor neurone signs. Autonomic features are uncommon.
Pseudobulbar Palsy VS Bulbar Palsy 1) degeneration or disturbance to : P: X, XI, XII, corticobulbar pathways sometimes VII B: rather than the to V,VII,X,XI,XII corticobulbar tracts 2) lower motor neurone signs P: absent B: present
Posterior cerebral artery territory infarcts Infarcts in the territory of the posterior cerebral arteries (PCAs) are common. Although associated clinical symptoms and signs are known, the mechanisms of stroke and the anatomical distribution of PCA territory lesions caused by the various stroke mechanisms are less well defined.
Forty-eight patients (61%) had infarcts limited to the PCA territory (pure PCA), while 31 (39%) also had infarcts in other territories (PCA+). Infarcts were in the cortical territory of the PCA in 47 patients (59%) and were cortical and deep in 32 (41%). Infarcts that were cortical and deep were more common in PCA+ lesions
Stroke mechanisms were embolism of cardiac origin (32 [41%]), proximal arterial disease (25[32%]), cryptogenic embolism (8[10%]), intrinsic PCA disease (7[9%]), vasoconstriction (4[5%]), and coagulopathy (3[4%]). Patients with cardiogenic embolism and intrinsic PCA disease often had pure PCA territory infarcts, while patients with proximal arterial disease more often had PCA+ infarcts. Visual abnormalities were present in 66 patients (84%). Motor weakness, cognitive and behavioral abnormalities, and ataxia were found in 20 patients (25%); only 12 (15%) had sensory signs.
CONCLUSIONS: The great majority of pure PCA and PCA+ territory infarcts are caused by cardiac or intra-arterial embolism. Intrinsic PCA disease, vasoconstriction, and coagulopathy are less common causes of infarction.
Villaret's syndrome Synonyms: Parotid space syndrome, posterior retroparotid space syndrome. A syndrome of ipsilateral paralysis of the ninth, tenth, eleventh, twelfth, and sometimes the seventh cranial nerves and the cervical sympathetic fibers. It is caused by a lesion in the posterior retroparotid space.
The clinical manifestations include Horner's syndrome and paralysis of the soft palate, pharynx, and vocal cords. In some cases there also may be paralysis of the superior constrictors of the pharynx, numbness of the soft palate, fauces, and larynx, loss of taste of the posterior one third of the tongue, and paralysis of the sternocleidomastoid and trapezius muscles.
Collet-Sicard syndrome Collet-Sicard syndrome Collective term comprising infectious disorders associated with encephalitis epidemica. Villaret's syndrome Villaret's syndrome A syndrome of ipsilateral paralysis of the ninth, tenth, eleventh, twelfth, and sometimes the seventh cranial nerves and the cervical sympathetic fibers.
Miller-Fisher Syndrome The Miller-Fisher syndrome triad – Ophthalmoplegia – Ataxia – Areflexia CSF protein is usually is elevated, but the NCS findings are more suggestive of axon loss than SD It is generally a benign disorder and does not require specific immune therapy A pure sensory form has been reported – The diagnostic criteria for GBS proposed in 1978 exclude this variant
Vasculitic Neuropathies Vasculitic neuropathies occasionally are mistaken for GBS Distinctions: – Systemic signs, including fever, are common – Sensory and motor involvement in the limbs usually is both distal in location and asymmetrical – Cranial nerve involvement, respiratory complications, and sphincter dysfunction are uncommon – CSF typically is normal (except with systemic lupus erythematosus) – NCS reveal changes suggestive of axon loss, rather than SD