Thursday, 19 January 2012

Can Cerebrospinal fluid pressure influence Optic nerve head neuropathy in Normal Tension Glaucoma?

Optom
Normal Tension Glaucoma is a type of Glaucoma without the common classical sign of Glaucoma pathogenesis- increased intraocular pressure (IOP). Increase in the pressure within the eyeball is the single most important factor that could indicate Glaucoma but it often times not enough to predict all types of Glaucomas. In Normal Tension Glaucoma, Optic nerve head neuropathy is the single most important sign of a pathology. The intraocular pressure (IOP) looks 'normal' but other signs like the dilation of the pupil & its apparent inability to react to light or acccomodation can be appreciated, especially when the disease has stayed for sometime...
Then comes the almighty question, why does the pupil becomes fixed & dilated when there is no 'high' IOP which should have compressed the Edinger Welpher pathway? Or how does the lamina cribosa death and optic nerve fibre appoptosis becomes possible in the presence of what appears to be 'normal' pressure?
Lets take a tour! The Optic nerve head tranverses through the the Optic disk via the lamina cribosa & terminates at the Optic chiasm. The lamina cribosa is the weakest portion of the sclera located at the posterior pole of the eyeball and perforated by the many fibres of the optic nerve. The optic nerve fibres @ this point (Optic disk area) is loosely attached to each other because of the absence of the cells of Muller. The weakness of the lamina cribosa area and the absence of the Muller cells in this position makes the optic disk head very vulnerable to inflamation and changes in pressure through the optic and neural pathways! The IOP of the eye is actually the pressure difference between the cornea and the atmospheric pressure. It is known as the transcorneal pressure. On the other hand, the pressure in the cranium and in the spinal cord is known as intracranial pressure (ICP). The later is a pressure difference between the atmosphere and the cranial compartments- the cranium and the vertebra.
Aqueous humor and the cerebrospinal fluid both similar in origin (a filtration substance) determines the IOP and ICP respectively. IOP should always be slightly higher than the ICP hence giving the optic disk head its classical depression. There is a homostatic arrengement as felt on the lamina cribosa and it is known as translaminar pressure, a pressure difference between the eyeball and the cranium and the spinal cord. Translaminar pressure has been attributed as the single most important phenomenon that discribes the stetching and subsequent atrophy of the lamina cribosa.
Translaminar pressure as felt on the lamina cribosa is calculated as (IOP-ICP). If the ICP is higher than the IOP a pseudo-tumor celebri or papilloedema or papillitis results. On the other hand, a very high IOP & low ICP results in Glaucomatous changes. It is attributed that the so called 'normal' tension glaucoma is as a result of the cushioning effect of the ICP on the lamina cribosa. The apparently 'high' IOP is cushioned by a not-too-low ICP causing a strain on the lamina cribosa to the point of nerve fibre cell apoptosis.
The average IOP is 16mmHg while the average ICP is 12mmHg, hence giving us a 4mmHg difference on the lamina cribosa. This gives the optic disk head a depression equivalent to the tranlaminar pressure difference of 4mmHg.
Even though glaucoma is not fully understood, I believe that ICP plays a role in normal tension glaucoma. It therefore becomes important to put such in consideration in diagnosis and management of this single most important silent thief of sight!
Thanks,
Dr Victor Ezebuiroh.
N/B: This article draws no financial interest anywhere.

Monday, 16 January 2012

Cataract, its treatment and the role of Optometry in Nigeria 3

Optom
Continuing, it is important to know the impact of cataract to the general population. Cataract functionally causes blindness in its final stages. About 17 million persons are blind from cataract only.
 In its early stage, especially when it affects one eye alone, the individual is almost symptomless. After sometime, depending on the causal agent and/or inducing agents, symptoms like photophobia, anisometropias, diplopia, secondary redness of the ipsilateral eyes, epiphora, itching, increased glare sensitivity etc could make the patient seek for medical attention. Most Optometrists in Nigeria become the first healthcare expert consulted. In later stages, other symptoms that are sight threatening starts showing up. Like secondary closed angle glaucoma, reduced vision on the ipsilateral eye with implications such as amblyopia in children etc; uveitis as the cataract intaracts with the iris and ciliary bodies etc. The last stage of such cataract, as I reinterated before, is functional and/or absolute blindness depending on the presence of conditions like induced glaucomas, secondary uveitis and bad surgery and/or followup.
Cataract becomes a bigger burden when it is bilateral. The symptoms show earlier and visual handicap is more obvious. It tends to affect activities of daily living among patients and renders individuals vulnerable. The most important symptom in this form of cataract is reduced bilateral vision especially at far. The use of glass correction is desirable at this early stage. Patients become sensitive to glare, and contrast sensitivty is said to be affected too. This patient is worried and wants to remove the source of discomforts in the eyes which includes itching, epiphora, sandy sansation etc. Bilateral cataract is very common in malnourished children, in Diabetics or in individuals taking very high doses of steroids for a long time or people exposed to very high radiations absorbed by the crystalline lens.
 Visual challenges posed by bilateral cataract is severe and sudden, not to mention the effect of colour vision challenges and seeing haloes around light that accompanies cataract development! Medical care is seeked earlier than in the case of monocular cataract.What does the Optometrist do? Since this individual had variously visited the chemist drugstores and/or the unorthodox medicine practitioner without any lasting solution, we can imagine what such individual's expectations would be. It becomes imparative for the Optometrist to run an extensive eye examination. First, do monocular and binocular visual acuity examination at far and at near. This should be followed by objective refraction using either a Retinoscope or using an auto-refractor.  After the refraction, patients are expected to be subjected to subjective refraction to ascertain whether glasses can reduce the induced blur. Then a suitable tonometer is used to check for induced increased intraocular pressure in the eye(s) with the cataract. Unless in eyes with associated Glaucoma, Optometric practioners are adviced to dilate the cataractous eyes with a dilating agent to access the extent of the cataract development.
One thing should remain obvious to the primary eye care practitioner- the patient's expectations! It is therefore important to have an open communication with your patient. Discuss surgery as the last option. Use glasses and drugs to try reduce blur, especially in its early stages. Use tints or photochromic lenses to manage glare, photophobia and effect of illumination. Reduce or remove symptoms like epiphora, itching and diplopia while encouraging patient to be coming for check-ups till cataract becomes ready for extraction. Meanwhile, the Optometrist should initiate a contact with a cataract surgeon as it regards this patient. The patient's medical records should be reviewed by the surgeon and an appointment is sheduled when appropiate. If the cataract is either drug induced or pathology related, a general practitioner or the personal Doctor of the patient is expected to play a significant role in managing such patients. Medical reports from the various healthcare practitioners should be made available and documented, as much as possible!
It is the role of the practitioner to know how desireous of surgery the patient is or should be. The rule of the thumb is that eyecare practitioner should never push a patient for surgery, except in children under 9 years or in traumatic cataract or the very hyper-mature cataract whose complications far outweighs post-surgical complications!
Drugs like N-Acetyl carnosine is reported all over the internet health world to be able to disolve cataract, others like Pirenoxine (Catalin), Potassium & Sodium Iodide combination (Vitrolent) are used to manage early cataract. It becomes imparative for the Optometrist to know which of the ophthalmic agents will be good for the patient and use it!
I will discuss Cataract surgery in my subsequent blog... Meanwhile, Happy new year readers!

Dr Okwudiri Victor Ezebuiroh

Note: This blog does not have any financial interest anywhere!