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Vertigo - still at bay, I can walk (like a crutacean) without nausea, a

lot less of a problem to negotiate where people are walking towards me,

that swooning feeling is gone

hearing - splendid, hear every word, have not had to have anyone repeat

themselves for days (that's the first time in more than four

years)

ringing in the ears - still there but, much much less so, I can enjoy

music and songbirds

constipation - without adding any more laxatives (just one cup of senna

tea at bedtime), I am starting to get caught up today (I'm still full of

it , just much less so), and the pain I have always (as long as I can

remember) had during a bowel movement is just barely there, as are the

excruciating spasms before and after, and I can go on with life, rather

than needing a lie down as before - it may help also that without the

vertigo I walk more and exercise more than I was able to

I think we should adapt the term Neurosy, really we are far from alike,

not cookie cutter illness, most of us have had enough of the hesitancy to

give a working diagnosis. We all have degeneration which have made

our bodies go wacko. Nitpicking, in the absence of a definitive

test is destructive to the spirit of the sufferrer. Each brain, is

completely different as are the levels of neurotransmitter needed to be

'normal' (whatever that is). Neurotransmitters or the absence

thereof in each category cause different symptoms in different people,

this is what we have in common, whatever clever terminology we use, we

are losing braincells, each of us slightly differrent, affecting those

neurotransmitters and their ability to regulate aspects of the CNS

(central nervous system), those in this group have autonomic problems

(some to mostly), and there is overlap.

There is no specific treatment, because there is no set pattern in which

each of us degenerates. The variables are extensive, including how

you live. Neurotransmitters (brain fog or I'd name them - dopamine,

norephenephrine, seretonin etc) are affected by touch, fear, joy, sensory

stimulation, medication, nutrition, light. The brain seems capable

of rewiring to a great degree, for as long as you have the energy and

determination to use it or lose it. Pain is also a byproduct of

neurotransmitter activity. Living with 'Neurosy' is a precarious

balancing act, with no set way to guide us. I've gathered more

'useful data from here than anywhere else on the net.

It would help to have a plain language cheat sheet - I found this on the

net last night, looks fascinating but it might as well be Aramaic, can a

few of you join me in deciphering it, that could be a good basis for the

badly needed neurosy cheat sheet.

_______

Maybe we could have a plain language project among ourselves.

Please fill in layman's terms after the '='

The differential diagnosis of parkinsonism

accompanied by

atypical features =

is broad and includes the Parkinsonism Plus

syndromes= constellation of

symptoms

(multisystem atrophies,

progressive supranuclear palsy, =

PSP

cortical-basal ganglionic

degeneration,

progressive pallidal atrophy,

diffuse Lewy body disease),

Alzheimer's disease with parkinsonian features,

Pick's disease,

hederodegenerative diseases ('s, Hallervorden-Spatz, Huntington's

disease, etc.),

and secondary parkinsonism = second

to another medical condition, medication or toxin (poisin)

(vascular, =

to do with blood and it's

circulation

drug induced, infection, =

prion disease, = like mad cow

disease

toxins,

cadmium would be an example

trauma,

= blow to the head for example

mass lesions,

= scarring all over (from demyelating

disease etc.)

hydrocephalus, =

water on the brain

hypothyroidism, =

underfunctioning thyroid

paraneoplastic, -

hepatocerebral degeneration, and -

syringomesencephalia). -

Of the various causes, the Parkinsonism Plus syndromes and secondary

parkinsonism are the most common.

Hederodegenerative

diseases are relatively uncommon, and this patient did not fit into

any of the recognized patterns of hederodegenerative disease. =

The patient's mild

subcortical dementia =

and the presence of

cerebellar signs =

did not fit the pattern expected for either Alzheimer's or Pick's

disease. Infectious possibilities include encephalitis lethargica,

= viral brain infection (leeping sickness)

HIV, = AIDS

syphilis, and

SSPE. =

In this case, serologic tests excluded syphilis and HIV infection, and

the clinical course and features were not consistent with encephalitis

lethargica or SSPE (which are rapidly progressive conditions). There was

no history of anti-psychotic or anti-emetic drug exposure, toxin (CO, Mn,

Hg, MPTP, CS2, methanol, cyanide) exposure, multiple head traumas,

multiple strokes, or metabolic abnormalities. Prion diseases, especially

Creutzfeldt-Jakob and Gerstmann-Straussler-Scheinker disease, present

with a more rapid, aggressive course and more profound dementia.

Neuroimaging excluded the possibility of hydrocephalus and mass lesions.

One might consider the possibility of normal pressure hydrocephalus,

consisting of the triad of dementia, gait disturbance, and urinary

incontinence. The mild subcortical dementia is consistent with this

diagnosis, but the lack of improvement of this patient's leg function on

lying down argues against it. Neuroimaging was not consistent with this

diagnosis.

The Parkinsonism Plus syndromes include an array of neurodegenerative

conditions characterized by parkinsonism plus other evidence of

neurological dysfunction as seen in our patient. In Diffuse Lewy Body

disease, parkinsonism is accompanied by cortical dementia with varying

levels of attention, early hallucinations, and psychosis. Autonomic

dysfunction is common, and

pyramidal signs =

may be seen, but

cerebellar dysfunction=

is not found. This patient's mild subcortical dementia is also not

consistent with this diagnosis. In cortical-basal ganglionic

degeneration, parkinsonism is accompanied by

ideomotor apraxias, =

the alien limb phenomenon, =

cortical reflex myoclonus, =

cortical sensory loss, =

marked asymmetry of involvement, =

and

focal rigidity =

and

dystonia =

with

contractures. =

None of these features was seen in this patient. In progressive

supranuclear palsy, parkinsonism is accompanied by a

prominent supranuclear gaze disturbance =

not seen in this patient.

Multisystem atrophy (MSA) is a

progressive, = gets worse

sporadic =

all over the place,

unpredictable

disorder characterized by

parkinsonism in association with varying degrees of

cerebellar, =

pyramidal, =

intellectual, = thought processing

ability

and

autonomic dysfunction. = unable to

control function which should not require thought (breathing, heart rate,

thermoregulation)

Classically, this includes three

separate entities -

Striatonigral degeneration (parkinsonism poorly responsive to levodopa

and frequently associated with cervical dystonia), =

Olivopontocerebellar atrophy (parkinsonism with cerebellar dysfunction),

=

and

Shy-Drager syndrome (parkinsonism with autonomic dysfunction). =

Because of the clinical overlap and common pathologic finding of an

intracytoplasmic oligodendroglial inclusion body, =

these entities are now lumped together. This patient best fit the

diagnosis of multisystem atrophy with evidence of parkinsonism,

cerebellar dysfunction, autonomic dysfunction, mild dementia, and

long-tract signs. =

Geez it can really make your head hurt!

aletta mes

vancouver, bc Canada

web:

http://aletta.0catch.com

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