The discovery of Parkinson’s disease (PD) is attributed to James Parkinson in 1817 when he called it shaking palsy. But Parkinson didn’t really discover the condition and it didn’t just suddenly appear in 1817. The condition actually goes back hundreds if not thousands of years in Traditional Chinese Medicine and Aryuvedic Medicine from India.


The Chinese character for shaking is wind so Traditional Chinese Medicine doctors referred to Parkinson’s disease as a wind condition which is the same as calling it a shaking condition.

The number of people afflicted with Parkinson’s disease (PD) in the United States alone is estimated to be somewhere between half a million to a million and a half. Despite decades and billions of dollars in research, however, the numbers are actually increasing. What is more alarming, is that there has been a significant increase in the incidence of early onset Parkinson’s.

Parkinson’s, Alzheimer’s and NPH

PD shares a peculiar relationship with Alzhiemer’s disease in that both can progress and develop similar signs and symptoms. Many years ago I discovered that they also share an association with normal pressure hydrocephalus (NPH). There weren’t enough brain scans when I started my research, now they are plentiful and the evidence is starting to mount about the connection between chronic cerebrospinal venous insufficiency (CCSVI) and NPH in Parkinson’s. Upright brain scans will be the wave of the future.

In addition to the role of CCSVI and NPH in PD, I believe PD is also associated with Chiari malformations. The cause of CCSVI, Chiari malformations and NPH is most likely the result of inherited genetic design problems in the drainage system of the brain. The other most likely cause is due to acquired disorders and degenerative conditions of the cervical spine, especially the upper cervical spine and base of the skull.

Primary Parkinson’s Disease

Currently primary PD is attributed to a decrease in dopamine production on the part of the substantia nigra. The reason for the decrease in dopamine production, however, is unknown. Supposedly the substantia nigra just goes bad one day and stops producing the way it should. But what causes such a small and highly localized area of the brainstem to suddenly start to go bad while the rest of the brain, for the most part, is working fine?


The picture in the upper left corner above is a sagittal (side view) of the brain stem with a cross section removed and layed out in the main picture. In this picture the substantia nigra (long grey area on either side of the cross section) is actually part of a system of interconnecting nerve centers, called the basal ganglia, and a router called the thalamus located in the core of the brain and brainstem that fine tunes the coordination of the movement of muscles. The basal ganglia take in and process information from different hard drives in the brain, called lobes, which among others include the motor and premotor cortex of the frontal lobe. The motor cortex sends the commands out for movement and the premotor cortex provides stored programs for that particular movement such as riding a bike or throwing a ball.

For another perspective the picture above is a coronal view (looking at the back of the head and removing a slice in the middle of the brain from top to bottom and from side to side. The first three structures listed are part of the basal ganglia and the substantia nigra and thalamus are also shown.

Memories of motor activities, however, reside in all the lobes of the brain, not just the motor cortex. The brain pictures riding a bike in the occipital lobes, at the rear of the brain, and stores long term memory of things about riding a bike in the temporal lobes, located on either side of the brain next to the ears, such as watch out for potholes and roads are slippery when wet. The parietal lobes, above the top of the ears, integrate and associate the information from smell, sight, sound, taste and touch. Some western athletes and all eastern martial arts use Zen visualization techniques, such as watching videos and mental imaging, to stimulate the occipital lobe to train muscles without using them.

Muscle movement requires fast timing and ultrahigh speed components. Consequently, in contrast to most of the brain, the interconnecting system of the basal ganglia uses a high speed neurotransmitter called acetylcholine.

The grey matter of the brain is for processing and integrating information and uses slower speed neurotranmitters such as dopamine. The substantia nigra also uses dopamine. We are now finding out that there is much more to dopamine than simply muscle movements and tremors. Among other things, it appears to play a role in long term memory.

The role of the substantia nigra and it’s neurotransmitter dopamine is to take the rough edges off movement by slowing down and smoothing out muscle activity which prevents overexcitation and tremors.


Again, the picture above shows the substantia nigra in blue on the brainstem and other structures of the basal ganglia.

The thalamus is the top of the brainstem which is located in the core of the brain and is extremely complex. But one of its primary roles is to serve as a router for distributing information about muscle movement to the different hard drives of the brain. The hypothalamus sits below the thalamus and also appears to play a role in muscle movement.

In contrast to the substantia nigra, which when malfunctioning produces resting tremors as seen in Parkinson’s, injuries to the hypothalamus appear to play a role in wild, erratic, exaggerated tremors such as those seen in Huntington’s Disease. Interestingly, Huntington’s disease is similar to PD in many ways and will be discussed separately on this website.

Secondary Parkinson’s Disease

Secondary PD is due to other causes rather than a decrease in dopamine production. It can be due to a decrease in the effect of dopamine on its target nerves. Secondary PD can also be caused by toxins such as, but not limited to, pesticides, excess manganese, alchohol, certain types of blood pressure medicine such as reserpine, psychotropic drugs and recreational drugs.

Secondary PD can also be caused by tumors and infarcts (dead tissue in the brain). It has always been associated with boxing, which used to be called pugilistic PD. For further information on this subject go to Parkinsons, dementia and neck injuries.

Parkinson’s and NPH

Decades ago, I suspected that PD was most likely due to venous drainage issues and NPH similar to Alzheimer’s. Among other things, CCSVI from back pressure against the venous drainage system of the brain can decrease the cerebrospinal fluid (CSF) pressure gradient and subsequent production of CSF. A decrease in the passive production of CSF would result in a decrease in CSF volume in the brain during upright posture. This could cause the brainstem to sink into the foramen magnum, which is called a pressure conus or Chiari condition.

Pressure conus and Chari conditions, in turn plug venous drainage outlets in the basement of the brain resulting in CCSVI. They also compress CSF pathways, resulting in impaired and sluggish CSF flow and subsequent NPH.

Chiari, NPH and Compression of The Substantia Nigra

The cerebellum and brainstem sit in what is called the posterior fossa (back of the skull). The foramen magnum lies on the floor of the posterior fossa. The brainstem lies parallel to and along the angle of what is called the clivus, which unites the occipital bone of the posterior fossa with the sphenoid bone in the middle fossa above, which is also part of the base of the skull. These structures are shown below in a sagittal view (the skull sliced in half from the front to back.)



The posterior fossa is covered by dura mata called the tentorium cerebelli, which means the tent of the cerebellum. In addition to a large portion of the brainstem, the posterior fossa also contains the cerebellum and most of the cranial nerves. The tentorium cerebelli separates the contents of the posterior fossa from the rest of the brain in the anterior and middle fossas above.

The picture below shows a coronal view of posterior brain compartments and the foramen magnum at the base.



Chiari conditions result in compression of the brainstem against the rim of the foramen magnum. Flexion type strains of the cervical spine, in which the head is in a position forward of the preferred perpendicular postural gravity line, traction the cord and brainstem toward the front edge of the foramen magnum. Normally, looking at person from the side, the mastoid bone behind the ear should line up over the malleoli (outside bone) of the ankle.

The picture above is a sagittal view of the lower brain, brainstem, skull and cervical spine. This picture shows the relationship of the brain stem to the foramen magnum which is immediately above the cervical spine.

A Parkinson’s patient’s posture is stooped due to the areas of the brain impacted on.

The substantia nigra is located in the pons area on the belly side of the brainstem making it equally susceptible to compression, Interesingly, the periaqueductal grey also lies nearby and plays a role in the freeze reflex, which could explain the frozen facial expressions and cogwheel rigidity-type movement seen in PD.

It is my opinion that CCSVI causes NPH and Chiari type conditions resulting in compression of the area of the brainstem that contains the substantia nigra. Furthermore, CSF entrapment from NPH can also cause increased pressure in the fourth ventricle which compresses important structures in the cerebellum such as the flocculonodular lobe.

The flocculonodular lobe is one of oldest parts of the brain in vertebrate evolution. Among other things, it controls truncal muscles related to posture, movement and balance and may play a role in stooped posture, rigidity of truncal muscles, problems with walking and loss of balance.

A variant of Parkinson’s disease of multisystem atrophy and is covered on a separate page.

Other pages of interest to the Parkinson’s page are cerebrospinal fluid, cerebellum, hyperintensity signals and diffuse hyperintensity signals.