Bifacial weakness (flow chart+table)

Rhaumatoid Arthritis

- Chronic systemic inflammatory disorder involving the joints

- Peripheral symmetrical non-suppurative arthritis

- Unknown cause (autoimmune)

- Onset : 30-50 years old

- F:M = 3:1

- Mnemonic for diagnosing RA: RF RISES

Ø Rheumatoid factor

Ø Finger / hand joints involved (>6weeks)

Ø Rheumatoid nodules

Ø Involvement of 3 or more joint areas

Ø Stiffness (morning) > 1 hour > 6 weeks

Ø Erosions on X-ray

Ø Symmetrical arthritis > 6weeks

Revised Criteria for the Classification of RA

1. Guidelines for classification a. 4 of 7 criteria are required to classify a patient as having rheumatoid arthritis (RA). b. Patients with two or more clinical diagnoses are not excluded. 2. Criteriaav a. Morning stiffness: Stiffness in and around the joints lasting 1 h before maximal improvement. b. Arthritis of 3 or more joint areas: At least 3 joint areas, observed by a physician simultaneously, have soft tissue swelling or joint effusions, not just bony overgrowth. The 14 possible joint areas involved are right or left proximal interphalangeal, metacarpophalangeal, wrist, elbow, knee, ankle, and metatarsophalangeal joints. c. Arthritis of hand joints: Arthritis of wrist, metacarpophalangeal joint, or proximal interphalangeal joint. d. Symmetric arthritis: Simultaneous involvement of the same joint areas on both sides of the body. e. Rheumatoid nodules: Subcutaneous nodules over bony prominences, extensor surfaces, or juxtaarticular regions observed by a physician. f. Serum rheumatoid factor: Demonstration of abnormal amounts of serum rheumatoid factor by any method for which the result has been positive in less than 5% of normal control subjects. g. Radiographic(X-ray) changes: Typical changes of RA on posteroanterior hand and wrist radiographs that must include erosions or unequivocal bony decalcification localized in or most marked adjacent to the involved joints.

- ^av Criteria a–d must be present for at least 6 weeks. Criteria b–e must be observed by a physician.

Parkinsonism

- A clinical syndrome characterized by (cardinal signs)

o Tremors (rest tremors)

o Rigidity (cogwheel)

o Bradykinesia (slowness in execution of motion / slow movement)

- Types of parkinsonism

o Primary parkinsonism = Parkinson’s disease (PD)

o Secondary parkinsonism – neuroleptics/antipsychotics (especially typical antipsychotics e.g. haloperidol), Wilson’s disease, stroke.

o Parkinsonism plus syndrome (PPS) – Progressive Supranuclear Palsy (PSP), Multiple System Atrophy (MSA).

[NB: since secondary parkinsonism is treatable thus it is important to recognized and accurately diagnose this.]

- Clinical diagnosis of PD:

o Asymmetrical signs of parkinsonism

o No clinical evidence of PPS & secondary parkinsonism

o Marked response to dopaminergic drugs

o Postural instability is the 4th cardinal sign, but it emerges late in the disease, usually after 8 years or more.

Proposed stages of Parkinson's disease (PD) based on extrapolations from pathologic, clinical and brain imaging studies. Broken black lines indicate that, by itself, Lewy (-synuclein) protofibril or fiber pathology is not sufficient to make the pathologic diagnosis of PD. Broken blue lines represent non-motor signs that usually precede clinical recognition of PD, including impaired olfaction, sleep and mood disturbances, and constipation. Broken yellow lines indicate that fluctuations may be less apparent in the late stages of PD. (Taken from Harrison's online)

- Treatment of PD:

o Early stage : dopaminergic drugs (i.e. dopamine agonist e.g. Mirapex / pramipexol & Requip / ropinirole)

o Late stage : brain surgery (Deep Brain Stimulation / DBS, pallidotomy & thalamotomy)

- Differences between PD & PPS

	Parkinson’s disease (PD)	Parkinsonism plus syndrome (PPS)
1	Response to dopaminergic drugs & brain surgery are good.	Poor response
2	Better long term prognosis (less aggressive course)	Poorer long term prognosis (more aggressive course)

Unilateral Facial Weakness (flow chart)

Case based learning (COPD)

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Speech disorder

Dysphasia / aphasia

Ø Impairment of the production and/or the comprehension of spoken or written words.

Ø Content of speech is abnormal. (language dysfunction)

Ø Assessment: mnemonic - CNS-RW

1. Comprehension

· 3 step instructions:

i. close your eyes/闭上您的眼睛(chinese simplified)/ अपनी आँखें बंद करो (Hindi)/ tutp mata (Malay)

ii. lift up your left hand /提起您的左手(chinese simplified)/ अपने बाएँ हाथ उठा (Hindi) / angkat tangan kiri (Malay)

iii. touch your left ear /接触您的左耳朵(chinese simplified)/ अपनी बाईं कान स्पर्श (Hindi)/ sentuh telinga kiri (Malay)

2. Naming objects

· Pen, key, book, card

3. Spontaneous speech

· Ask about his day, family, visitors, occupation

4. Repetition of sentence

· I want to go to the toilet /我想要去洗手间 (chinese simplified)/ मैं शौचालय जाना चाहती हूँ (Hindi)/saya nak pergi ke tandas (Malay)

5. Writing

· Write a given sentence e.g. regarding residence – I live in an apartment at Damansara Utama./ 我在公寓居住在damansara utama(chinese simplified)/ मैं एक अपार्टमेंट में damansara utama में रहते हैं (Hindi)/Saya tinggal di Damansara Utara dalam sebuah rumah bertingkat.(Malay)

· Write out a given instruction – “lift up your left hand” /提起您的左手(chinese simplified)/ अपने बाएँ हाथ उठा (Hindi) / angkat tangan kiri (Malay)

Ø Types of dysphasia :

Clinical features	Expressive (Broca’s) dysphasia	Receptive (Wernicke’s) dysphasia	Conductive dysphasia	Nominal dysphasia
Comprehension	Normal	Impaired	Normal	Normal
Naming objects	Impaired	Impaired	Impaired	Impaired
Speech	Telegraphic (staccato speech)	Paraphasia Neologism	Paraphasia Neologism	Lack nouns
Repetition	Impaired	Impaired	Impaired	Normal
Writing	Impaired	Impaired	Impaired	Pauses (lack nouns)
Spontaneous	Non-fluent (mute if severe)	Fluent	Fluent	Pauses
Site of lesion	Left inferior frontal gyrus	Left superior temporal gyrus	Left arcuate fasciculus	Left temporal lobe

Dysarthria

Ø Imperfection in articulation of speech.

Ø Content is normal.

Ø Subtypes:

o ”Hot potato” speech = Pseudobulbar dysarthria

o Nasal speech = Bulbar dysarthria

o Scanning / staccato speech(syllable by syllable) = Cerebellar dysarthria

o Monotonous, soft speech = Parkinsonian dysarthria

Dysphonia

Ø Impairment in production of voice (soft / hoarse voice)

Ø Content of speech is normal.

Ø E.g. vocal cord palsy

Speech disorder (flow chart)

Knowing the language of a disease

Palpation of the radial pulse is often one of the first things that doctors do when examining a patient. The pulse is examined for its rate, rhythm and character. The peripheral pulses are also examined to see if they are equally and symmetrically felt. Each of these aspects of the pulse can offer diagnostic clues to the doctor who understands the language of diseases.

Here is an example of how an examination of the pulse allowed one doctor to make a diagnosis that startled his students.

Dr X was told that a particular patient had a heart murmur. He was not allowed to auscultate the patient to determine anything more about the murmur. He was only allowed to palpate the patient's pulse. Thirty seconds after examining the patient's pulse, Dr Sandy said: This patient has aortic regurgitation. His students, new to clinical medicine, were all stunned.
They asked him: How did you correctly diagnose a valve abnormality in the heart by simply feeling the pulse?
Elementary, my dear students, Dr X replied. I noted that the pulse was of a collapsing nature. Only a few conditions are associated with a collapsing pulse and a heart murmur. Aortic regurgitation is one of them.

Do you know what cardiac abnormality to diagnose when:

1. The pulse is of small volume and rises slowly to its peak? This kind of pulse is called the anacrotic pulse.

2. The pulse has two distinct peaks during systole? This kind of pulse is called the bisferiens pulse.

3. The pulse disappears during inspiration? This kind of pulse is called the paradoxical pulse.

Brother & Sister Liver

A review article in the New England Journal of Medicine tells us about the increased cardiovascular risk in people who have non-alcoholic fatty liver disease. Non alcoholic fatty liver disease comprises a spectrum of conditions where fat accumulates in the liver to produce conditions like hepatic steatosis (simple accumulation of fat in the liver), non alcoholic steatohepatitis (or NASH, where the fat accumulation is associated with hepatitis) and cirrhosis liver. NASH is the condition where there is overt inflammation in the liver caused by the fat. It is this inflammation, overt or subclinical, that is believed to be responsible for producing those inflammatory cytokines that damage the liver (leading to cirrhosis) and the endothelium of blood vessels (leading to atherosclerosis and ischemic organ damage). Even before overt cardiovascular disease develops, people with NASH have subclinical evidence of increased atherosclerosis in their vessels as shown by an increased carotid intimal-medial thickness.

The diagnosis of non alcoholic fatty liver disease is often made by an ultrasound examination of the liver. The diagnosis of NASH is made when, in addition, there are elevated liver enzymes. Of course, one needs to exclude other causes (for example, viral causes) of elevated liver enzymes. Speaking of elevated liver enzymes, studies have found that an elevated gamma glutamyl transferase is more significantly correlated with cardiovascular disease than elevated levels of alanine transaminase.

Many people with non alcoholic fatty liver disease have features of the metabolic syndrome (abdominal obesity, hypertension, atherogenic dyslipidemia and abnormalities in plasma glucose). The metabolic syndrome has within it many risk factors for cardiovascular disease and so, it is not surprising that the treatment of non alcoholic fatty liver disease also focuses on treating these risk factors. In particular, treatment with insulin sensitisers (Metformin, Pioglitazone) are recommended for glucose abnormalities associated with non alcoholic fatty liver disease. Life style modification for weight reduction and to reduce abdominal obesity is also to be emphasised. Pioglitazone and Vitamin E may also be useful in reducing the inflammation and fat in this condition even though there is no evidence yet that these can prevent cirrhosis.

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