Akinetic-rigid Parkinson's Disease

       My Parkinson's symptoms seem to be different almost everyday. Some days I am dog tired and other days I seem to have some energy.  It is difficult to make plans too far in advance because I never know what my Parkinson's will be like on any given day.  My worst Parkinson's symptoms are being off balance and overwhelmingly sleepy!!  I don't know if it is a Parkinson's symptom or  not but I now have such vivid and bizarre dreams! Perhaps it is the liquid medical marijuana that I take at night to help me sleep!!

My sciatica,  however, seems to stay the same.

It is just pain all of the time unless I take Tylenol or a muscle relaxer. I have spoken to several people who have Parkinson's and many also have sciatica. I asked the doc this morning and he said there is no corelation. 

 Today I saw a new neurologist at a city hospital.  He diagnosed me with Akinetic-rigid Parkinson's.  He told me that there are two different types of Parkinson's disease. One is predominantly driven by tremors and the other is what I have. The Akinetic-rigid type of Parkinson's is characterized with slow and small movements and difficulty with getting up and down. I tried to google this type of disease and I didn't find too much information. The doc told me that this type of Parkinson's carries a better prognosis but it is still Parkinson's and it is still a degenerative disease.  He told me that there are 5 stages of Parkinson's and I am between stage 2 and 3(not good). I have problems with balance so he increased my carbidopa levodopa to two tablets three times a day. He told me that there is no definitive cause for this type of Parkinson's and it equally affects males and females.  I found the information below on webmd.




In patients above 40 years of age neurodegenerative disease is the commonest etiology of akinetic rigid syndrome. In this group idiopathic Parkinson's disease (PD) needs to be differentiated from other syndromes as it carries a better prognosis. These diseases are slowly progressive and have characteristic extra pyramidal signs, progression and associated neurological involvement. The differential diagnosis may be considered depending on whether the disease is symmetrical [multiple system atrophy (MSA), progressive supranuclear palsy (PSP)] or asymmetrical [Parkinson's disease (PD), corticobasalganglionic degeneration (CBD)]

Rigidity

The rigidity of IPD is “lead pipe” in character—that is, constant throughout a full range of passive movement. If a postural tremor is superimposed it takes on a ratchet characteristic described as “cogwheel” rigidity. The presence of rigidity can result in complaints of muscular aching and stiffness of limbs and back and, in the absence of tremor, some cases may initially be referred to a rheumatologist in error. The majority of patients have rigidity on examination, especially if synkinesis of the opposite limb is performed; the increased tone is often unilateral at presentation spreading to become bilateral over 3–5 years, but maintaining an asymmetrical emphasis.

The rigidity initially targets limbs but later spreads axially. A predominant involvement of limb and trunk flexors leads to characteristic “dystonic” posturing with trunk, neck, and arm flexion, and foot inversion. The rigidity is abolished by sleep and in 80% of cases responds well to dopaminergic agents.

Slowness

Fifty per cent of IPD patients complain of slowing up at presentation. Writing becomes smaller (micrographia). Later on they develop difficulty washing, feeding, dressing, and turning in bed, but these functions are rarely problematic at presentation. Loss of facial expression occurs early, causing social embarrassment, while decreased eye blinking, hypophonia, and impaired swallowing leading to sialorrhoea are later features. The slowness of IPD involves both initiation and execution of movements, particularly sequential and volitional actions. Characteristically the patient will perform finger–thumb opposition movements well a few times and then the amplitude will diminish and motor arrest may occur. A common clinical mistake is to allow the patient insufficient time to overcome their bradykinesia when testing power and so eliciting artefactual weakness. Limb bradykinesia generally responds well to dopaminergic agents.

Gait and postural reflexes

While gait is frequently slowed at presentation, this first manifests as a non-specific feeling of taking longer to get around or of one leg occasionally dragging or catching. Reduced arm swing on the affected side is usually evident. Later a tendency to shuffle develops, followed by gait initiation difficulties, freezing, and festination—involuntary acceleration while walking. At the same time, postural instability and retropulsion lead to difficulties turning and rising from a chair. While early slowing of gait responds to dopaminergic agents the later complications do not, though they may be helped by the presence of external cues—such as walking across lines or listening to a metronome ticking or marching music on a walkman tape.

Ocular movements

Pursuit eye movements are preserved though later may become hypometric with saccadic intrusion. Reflexive saccades to targets remain intact but formal testing of remembered saccades to an occluded target or anti-saccades reveals slowing. A frank supranuclear gaze problem is rarely seen but has occasionally been described in association with diffuse Lewy body disease. Restricted voluntary upgaze and convergence can, however, be seen and, indeed, is present in a minority of elderly normal subjects.

Voice

This initially becomes quiet and speech loses its natural cadence and prosody. Later lingual and labial bradykinesia leads to problems with articulation and speech becomes indistinct. Pallilalia is a feature of end stage disease.