seizures are electrically induced in anesthetized patients for therapeutic effect

Electroconvulsive therapy (ECT), formerly known as electroshock, is a psychiatric treatment in which seizures are electrically induced in anesthetized patients for therapeutic effect. Its mode of action is unknown.[1] Today, ECT is most often recommended for use as a treatment for severe depression that has not responded to other treatment, and is also used in the treatment of mania and catatonia.[2] It was first introduced in 1938 by Italian neuropsychiatrists Ugo Cerletti and Lucio Bini, and gained widespread use as a form of treatment in the 1940s and 1950s.[

Mechanism of action

The aim of ECT is to induce a therapeutic clonic seizure (a seizure where the person loses consciousness and has convulsions) lasting for at least 15 seconds. Although a large amount of research has been carried out, the exact mechanism of action of ECT remains elusive. ECT doctors claim it may "jumpstart the brain", helping boost neurotransmission, while others like Peter Breggin,[citation needed] claim it causes the "euphoric" effects similar to the effects found in "closed head injury" or people with fresh traumatic brain injury.

VASCULAR, or multi-infarct, dementia

VASCULAR, or multi-infarct, dementia is caused by the accumula-tion of small (lacunar) or large infarctions, often in conjunction with deep white-matter ischaemia. These changes are best seen on MRI using T2-weighted sequences (figure 5)

cholinesterase inhibitors for anti dementia

Acetylcholine is the neuro-transmitter most involved in creating new memories. As dementia progresses, acetyl-choline levels fall steeply. This decline is corrected by cholinesterase inhibitors, which boost the levels of available acetylcholine.

Three cholinesterase inhibitors are approved for treatment of Alzheimer's dis-ease: donepezil (Aricept), galantamine (Reminyl) and rivastigmine (Exelon). Mar-keting claims aside, there is little to distinguish between them in terms of efficacy.

Starting on half the rec-ommended dose reduces side effects (nausea, loose bowel motions, leg cramps and vivid dreams), which often settle within weeks. Gas-trointestinal symptoms are also mitigated by the use of Exelon patches. Cholinesterase inhibitors can aggravate peptic ulcer, asthma and bradycardia. The last of these is a particu-lar concern in patients taking beta blockers, which may need to be stopped. They also prolong the action of succinylcholine and other muscle-paralysing agents. Treatment must therefore be stopped briefly a day before surgery requir-ing the use of such agen

Heart sound splitting

Splitting.
Splitting of the first heart sound is usually not detectable clinically; however, when it occurs it is
most often due to the cardiac conduction abnormality known as complete right bundle branch block.

Increased normal splitting (wider on inspiration) of the second heart sound occurs when there is
any delay in right ventricular emptying, as in right bundle branch block (delayed right ventricular
depolarisation), pulmonary stenosis (delayed right ventricular ejection), ventricular septal defect
(increased right ventricular volume load), and mitral regurgitation (because of earlier aortic valve
closure, due to more rapid left ventricular emptying).
In the case of fixed splitting of the second heart sound, there is no respiratory variation (as is
normal) and splitting tends to be wide. This is caused by an atrial septal defect where equalisation
of volume loads between the two atria occurs through the defect. This results in the atria acting as a
common chamber.
In the case of reversed splitting P2 occurs first and splitting occurs in expiration. This can be due to
delayed left ventricular depolarisation (left bundle branch block), delayed left ventricular emptying
(severe aortic stenosis, coarctation of the aorta) or increased left ventricular volume load (large
patent ductus arteriosus). However, in the last-mentioned, the loud machinery murmur means that
the second heart sound is usually not heard.

Alzheimer's disease diagnostic criteria

Alzheimer's disease diagnostic criteria



• Memory impairment and one or more of:

— aphasia

— apraxia

— agnosia

— disturbance in executive functioning (ie, planning,

organising, sequencing, abstracting).

• These cognitive changes are sufficient to cause significant

impairment in social or occupational functioning and

represent a significant decline from a previous level of

functioning.

• These changes are not due solely to delirium or other

neurological conditions (eg, cerebrovascular disease) or

systemic conditions (eg, neurosyphilis).

• The course is characterised by gradual onset and continuing

decline.

Dementia lab screening

A typical dementia laboratory screen includes: • FBE. • Urea and electrolytes. • Thyroid function tests. • Lipids. • B12, folate. • Syphilis serology. • Brain CT scan.

It is unlikely that this screen will uncover treatable causes of demen-tia. These are rare. People with brain tumours or normal-pressure hydrocephalus usually present with localising signs and symptoms. With rare exceptions, a routine laboratory screen uncovers inci-dental pathology that cognitively impaired patients have failed to report (eg, hypothyroidism), together with pathology due to self-neglect (for example, iron-defi-ciency anaemia). Identifying and treating these conditions may not reverse the dementia but will improve functional capacity, lessen

carer burden and delay admission to residential care. A brief physical examination will reveal treatable vascular risk factors (eg, hypertension) and pointers to self-neglect (eg, poor hygiene and weight loss). Brain scans are often normal in cases of mild to moderate demen-tia. Eventually, people with demen-tia show generalised atrophy, irre-spective of cause. In earlier stages, medial temporal lobe atrophy is typical of Alzheimer's disease. Spe-cial views must be requested to see these changes clearly. In later cases, bilateral temporo-parietal deficits are characteristic (figure 2). Focal frontal and/or temporal atrophy is typical of frontotempo-ral dementia, while infarctions and deep white-matter ischaemia are typical of vascular dementia. Func-tional imaging using PET or single-photon emission computed tomog-raphy can be useful in cases of diagnostic uncertainty.

Pathology PATHOLOGICALLY, Al-zheimer's disease is charac-terised by the presence of amy-loid plaques and neurofibrillary tangles, initially in medial temporal lobe struc-tures and later more diffusely. Amyloid protein is ubiq-uitous in human tissues. Its role is unclear but in Alzheimer's disease its struc-ture is changed and it pre-cipitates in an insoluble form as extracellular plaques (figure 3). This toxic, abnormal form of amyloid results in cell death. Deposits are present within the brain at least 10 years before symptom onset. Amyloid can now be imaged

directly in selected research centres using radio-ligands (figure 4). Neurofibrillary tangles are intracellular inclusions com-posed of tau protein. Tau

gives structural support to channels transporting cellu-lar nutrients and neurotrans-mitters along axons In Alzheimer's disease, fibril hyperphosphorylation

results in a loss of structural rigidity and the formation of tangles. Neither tau nor amyloid pathology are unique to Alzheimer's disease. Amy-

loid changes are also associ-ated with vascular demen-tia and dementia with Lewy bodies, whilst tau pathology is seen in frontotemporal dementia.

Dementia versus normal ageing

Diagnosing dementia

Alzheimer's disease

fore be more impaired. Currently about 30% of residents of low-care facilities, and 80% of those in high care facilities, have significant degrees of dementia. These propor-tions will increase in the future. It is vital that GPs be familiar with the signs, symptoms and com-plications of dementia and with its treatment. In the past, doctors were reluctant to share diagnoses with families, let alone patients, on the grounds that dementia was an untreatable, progressive and thus unspeakably depressing condition. They feared that families would

react adversely to a diagnosis, but in fact most welcome a clear expla-nation for the changes in cognition, personality and behaviour that have so perplexed and frustrated them. Frank, sympathetic disclosure alerts spouses and children to the need to monitor personal care and safety more vigilantly. They will also respond less critically when con-fronted with memory lapses, self-neglect and challenging behavioural symptoms. There is now a trend to share information with patients, espe-cially those in the early stages of dementia, who have insig

7Ds of breast examination

BREAST EXAMINATION


Ask for chaperone
Remove clothes from waist up
Put patient in a lying position with 45 degree angle
Ask patient to point with 1 finger where exactly is the lump
Inspect the patient’s breast, compare both breasts
Tell patient to raise both hands, to see if there is any attachment
Check the level of both nipples, same or not
Any accessory nipple or deviation
Any apparent erythema, fissure in the nipple, any secretion or blood from the nipple
Look for peau d’orange
Tell patient to put her hands on the hips and press à to fix the pectoralis muscle
Come more closely and look at the nipple, look for 7D:
- Discolouration
- Discharge
- Depression
- Deviation
- Displacement
- Distraction
- Duplication (any double nipple)

Comment if both breasts are symmetrical in size, shape
Take permission to touch the breast
Palpation of the normal breast
Examine the left breast, ask patient to raise her left arm behind the head
Examine the right breast
With the tips of the finger start from midline of the chest to the breast around then armpits
Examine the lump: size, surface, edge, consistency, pulsation, tenderness if related to the skin and underlying muscle, fluctuant or not, transilluminate or not
Palpate the 5 areas of lymph node in the axilla à (anterior, posterior, lateral, medial, apical), supraclavicular fossa & cervical lymph node
Well defined lump, not painful, 1 cm, more or less solid in the right breast
Rapidly check all lymph nodes of the body
Chest, heart, abdomen

Coincide with benign lesion called fibroadenoma
Refer to the radiologist for a simple procedure to confirm the diagnosis à USG with a guided percutaneous core biopsy if needed, will be decided by the procedural radiologist

ALL neurodegenerative forms of dementia are relentlessly progressive

Summary

ALL neurodegenerative forms of dementia are relentlessly

progressive. After the diagnosis is confirmed the course is

palliative. Medications may help symptoms but not the underlying

pathological process.

Support networks such as Alzheimer's Australia and

Metropolitan Domiciliary Care should be available to all patients

diagnosed with dementia. The key to keeping these people at

home within the family unit is providing adequate support to the

carers.

At the current autopsy rate, little will be learnt as to correlating

clinical with pathological findings. Perhaps as new imaging

techniques filter down we may become better at antemortem

diagnosis.

In the meantime we should return to historic practices of

realising the importance of postmortem diagnosis to inform the

family of future risks and primary prevention methods, and to

provide practitioners with diagnostic certainty.

In SA the Brain Bank does just this, although it is societal

values that often prevent brains from reaching this valuable

resource. Educating practitioners and family members about the

importance of services like these will see them survive to provide

essential information and improve the understanding and delivery

of health services in the future.

Is your anxiety linked to place, situation, physical Sx, thought stick, ritual to stop

Questions to ask about panic disorder, OCD and GAD

For anxiety disorders generally

• Is your anxiety or worry predictable? Does it only ever happen in certain situations

or places, like shopping malls?

• Does your anxiety or worry ever go away?

• Do you have anxiety attacks that come from out of nowhere?

• Is your anxiety or worry linked with physical symptoms such as a racing heart,

shortness of breath and sweating?

• Do you always feel wound up, on edge or nervous?

• Do you have any thoughts that come into your head and make you worry?

• Are there rituals or things you have to do to stop feeling worried or to prevent a

catastrophe?

For GAD

• Do you often feel anxious, nervous, worried or on edge?

• How often? Most days, some days or almost never?

• How difficult is it to control your worry? Very, a bit or not very difficult?

• Is your worry realistic or reasonable or is it out of control?

• What do you worry about? One thing, or many things? Do you worry a lot about

too many things?

• Does your worry or anxiety help you, or does it interfere and slow you down?

• Do you have trouble relaxing?

• Do you feel fidgety because of your worry?

• Do you find you are becoming easily annoyed or irritable?

• Does it feel like something terrible might happen?

SSRIs and suicide

SSRIs and suicide

SSRIs are less toxic and have fewer unwanted effects than tricyclic antidepressants but it seems they may, paradoxically, induce suicidal behaviour in the young.
It is not easy to establish whether this is true because depression also increases suicide risk and the data are contradictory. Pharmaco-epidemiological and ecological studies suggest that increased use of SSRIs may have resulted in a reduction in youth suicide, and that SSRIs are not taken more often than expected by young suicide victims. However, a review of 24 controlled trials with more than 4400 children and teenagers by the US Food and Drug Administration showed a small (2%) short-term increase in the incidence of suicidality (suicidal thoughts or attempts) in those receiving antidepressants (mostly SSRIs) compared with placebo. There were no completed suicides and this result was not replicated when questionnaires, rather than reports from parents or children, were used as the basis for information. According to this research, 50 teenagers need to be treated for one to develop suicidality attributable to the antidepressant.

The mechanisms underlying this phenomenon are unclear but SSRIs, particularly paroxetine, can induce akathisia, agitation and irritability — so-called ‘activation' — and this may be an indicator of increased suicide risk.

Teenager depression - mood, interest, appetite, sleep, energy, concentration, suicide

the teenager unhappy or irritable? OR Does the teenager show loss of interest or pleasure in most activities?

(This happens most of the day, nearly every day for at least two weeks)

Yes

Does this teenager show at least five of the following?

� Depressed or irritable mood

� Loss of interest in activities

� Significant weight or appetite change

� Insomnia or hypersomnia

� Psychomotor agitation or retardation

� Fatigue or loss of energy

� Feelings of worthlessness or guilt

� Diminished ability to think or concentrate, or indecisiveness

� Recurrent thoughts of death or suicide

Yes

Do these symptoms cause clinically significant distress or impairment in social, school or family functioning, and are they not due to bereavement?

Yes

Is there a history of manic or hypomanic symptoms (eg, periods of elation or elevated mood) or a family history of bipolar disorder?

No Yes

Major depressive disorder is likely

Figure 1: Is this teenager depressed?

Consider other diagnoses or problems

Consider the possibility of bipolar disord

It is therefore critical to inquire as to the presence of past hypomania in every person presenting with depression, otherwise the possibility of a bipolar diathesis is easily missed.

It is therefore critical to inquire as to the presence of past hypomania in every person presenting with depression, otherwise the possibility of a bipolar diathesis is easily missed.



What are mania and hypomania? Mania is defined on the basis of symptoms and signs that are out of character for the individual and usually occur in discrete episodes (table 1). In the DSM-IV the diagnosis of mania requires the persistence of euphoric mood for a period of at least seven days, during which a minimum of three additional symptoms (four if mood is mainly that of irritability) are present. Technically, the predomi-nant mood is either that of excessive happiness, described as euphoria, or, alternatively, feelings of irri-tability. In practice, individ-uals will often describe feel-ing “pumped up” and “energised” or “wired”, with a notable increase in drive and goal-directed activ-ity that often results in increased pleasure-seeking behaviour. Other features include a decreased need for sleep, racing thoughts and dis-tractibility. Not surprisingly, many of these symptoms, and risk-taking behaviour in particular, can result in sig-nificant social or occupa-tional impairment, with potentially painful conse-quences such as risk to health, livelihood or reputa-tion. The symptoms and signs of mania can be conve-niently remembered using the mnemonic FIDGETS. (table 2). Hypomania is defined along the same lines as mania with regard to signs and symptoms, but the term is usually used to describe briefer periods of mood dis-turbance that generally incur less functional impairment than in mania. The DSM-IV employs a somewhat arbi-trary cut-off of four days' duration to define hypomania, but in practice this is often difficult to apply. In practice the diagnosis of hypomania is less reliable than that of mania or depression and it is seldom spontaneously reported because it is usually mild and transient and construed as a pleasant experience. People with bipolar disorder often consider periods of hypomania to be ‘normal' and understandably regard them as desirable, and rarely present clinically with such symptoms. However, it is important to remember that hypomanic symptoms are, more often than not, functionally dis-abling and that it is critical

to screen for manic or hypo-manic symptoms even in patients presenting with depression. This is important because identifying previous hypomania distinguishes a subsequent depressive episode as bipolar rather than unipolar. It is therefore critical to inquire as to the presence of past hypomania in every person presenting with depression, otherwise the possibility of a bipolar diathesis is easily missed.

What is bipolar depression? Although mania is the hall-mark of bipolar disorder, it is the depressive phase of bipolar illness that is the pre-dominant component of this illness both in terms of time spent unwell and the associ-ated functional disability. This bias in morbidity towards depression is even more pronounced in bipolar II disorder compared with bipolar I disorder. Like unipolar depression, bipolar depression is associ-ated with an increased risk of suicide. However, bipolar depression differs from its unipolar counterpart in sev-eral ways. An abrupt, earlier age of onset is more likely in bipolar depression, com-pared with a more gradual onset and offset in unipolar depression. A family history of bipolar

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