Elderly patient with

This case quite refers to the classical presentation of Normal Pressure Hydrocephalus. In real life, it may not be such a straight forward diagnosis.With an elderly patient, there are a number of differentials which you need to consider. There are a number of diagnostic criteria for iNPH and you can find more in the standard textbook. However here a more practical approach has been discussed

The Hakim's Triad:

The triad of progressive gait apraxia, cognitive deficits, and urinary incontinence in the context of relative ventricular enlargement and a cerebrospinal fluid (CSF) pressure less than 20 cm H2O. But it should be noted that you don't need to have this complete triad for a patient to have NPH!!

Here I also wish to add about  asymptomatic ventriculomegaly with features of idiopathic normal pressure hydrocephalus on MRI (AVIM)  AVIM.  Regarding radiological findings ,the finding of disproportionately enlarged subarachnoid space hydrocephalus without neurologic symptoms has been termed asymptomatic ventriculomegaly with features of idiopathic normal pressure hydrocephalus on MRI (AVIM). It is felt by some authors that AVIM is actually a pre-clinical form of idiopathic normal pressure hydrocephalus
 

Clinical differential diagnosis includes vascular dementia and atypical parkinsonian disorders, e.g. progressive supranuclear palsy and multiple system atrophy - Parkinsonian type (MSA-P) 32.

The possible imaging differential spectrum includes:

• Can it be Alzheimers?
•  Is it vascular dementia or atypical parkinsonian disorders, e.g. progressive supranuclear palsy and multiple system atrophy - Parkinsonian type (MSA-P) 

How the patient present:Each and every sign and symptom needs careful evaluaion

• Talking about cognitive decline, we need to evaluate what we actually mean by it? It can range from mild cognitive impairment to full blown dementia
• The distinction between cortical and subcortical syndromes of dementia is controversial. Clinical reports suggest that subcortical syndromes (NPH ,may also be seen in Parkinson;s) involve less severe intellectual and memory dysfunction and lack the aphasia, agnosia, and apraxia typical of the cortical dementias (eg, dementia of the Alzheimer type) . (Table 1)
• Presence of cortical signs such as aphasia or agnosia should raise suspicion for an alternate pathology such as Alzheimer disease or vascular dementia. 
• It is important to keep in mind that it is not uncommon to have comorbid pathologies in elderly. 
• In memory loss, we need to see if it is short or long term memory loss. 
• With gait impairment, we need to thoroughly see what impairment it really is. Parkinson disease and NPH may present in a similar, but distinct manner. Start hesitation and freezing episodes can occur in NPH, often mimicking the gait in Parkinson disease. In contrast to Parkinson disease, rigidity and unilateral rest tremor are less commonly observed 

How to differentiate it from dementia?
I'm sharing the tables. Please take proper history ,did the patient started with gait apraxia or is it the cognitive decline which is predominant? In NPH gait apraxia should be the first one to notice 

• Early postural impairment, falls, oculomotor impairment, and/or hallucinations are generally inconsistent with the diagnosis of NPH and may suggest progressive supranuclear palsy (PSP) and dementia with Lewy bodies (DLB)underlying NPH mimic
  
• Always note, did your patient suffer from cognitive decline first/ there are more s/s of cognitive decline. That would rather point towards other causes of dementia e.g Alzheimer's
  The “frontal–subcortical” dementia pattern of NPH affects processing speed, attention, working memory, and executive function, but spares “cortical” capacities such as praxis, speech, sense modalities, recognition, and long-term memory.
  
• Please note patients with NPH have tendency to enter delirium beware of it and don't consider it a part of what they are feeling if the care giver notifies you about a change in pt behaviour 

Radiological findings
Lateral and 3rd ventricle affected more
Check the sylvian fissure for swidening

There is disproportional size of basal and Sylvian and parasagittal CSF fissures basal and Sylvian being wide while parasagittal being narrow if present at all. wide aqueduct with a significant signal void in it from high-speed flow on T2-weighted images
Narrow subcallosal angle less than 90 degrees
Crowding at vertex

Here I want to also mention about DESH.  Disproportionately enlarged subarachnoid space hydrocephalus (DESH) is a pattern of communicating hydrocephalus characterized by crowding of the sulci superiorly near the vertex accompanied by enlargement of CSF spaces more inferiorly, particularly in the Sylvian fissures 1. It is a prominent feature of idiopathic normal pressure hydrocephalus (iNPH) and is a central component of the Japanese iNPH diagnostic guidelines 

(Special courtesy radiopaedia.org)

Seizures: Yeah there can be partial seizures

Gait differentials:

Typically, gait ataxia is the most useful ,early ans most common indication of NPH.
Patients report unsteadiness but no vertigo or illusion of motion, lightheadedness, or weakness. It may be difficult for both physician and patient to distinguish the gait of early NPH from so-called senile gait or very early parkinsonism. As the gait deteriorates, which may occur over months or years, the base of the gait widens and its speed and fluidity decline. Like the gait of patients with Parkinson’s disease, stride length shortens (marche a petit pas) and gait speed slows. There may be some degree of shuffling, decreased floor clearance and difficulty turning. Unlike the gait associated with Parkinson’s disease, cogwheel rigidity, if present, is mild compared to the degree of gait difficulty. Other features that distinguish NPH from Parkinson’s disease are the absence of significant resting tremor or drooling and failure to improve when levodopa is administered. Cerebellar ataxia can be distinguished from NPH by the presence of dysarthria, gazeevoked nystagmus, and appendicular dysmetria, none of which are typical of chronic hydrocephalus. Gait apraxia may worsen to the point of “magnetic gait,” and patients appear to have forgotten how to take a step or even to stand.

 When gait disturbance is the predominant symptom of NPH, it implies an improved chance of responsiveness to CSF shunting. Furthermore, gait abnormality is the most likely component of the symptom triad of NPH to improve with CSF diversion, and the absence of gait ataxia predicts poor responsiveness to shunting. Although there is some correlation between ventricular size and gait apraxia, the relationship is not entirely reliable. Some patients may exhibit severe gait impairment with only mild ventricular enlargement while others with very large ventricles walk surprisingly well. 

Cognitive impairment:

NPH can be considered as a reversible cause of dementia however If the dementia is severe, CSF shunting may result in little or no improvement.
Vascular dementia can be distinguished by magnetic resonance (MR) imaging of the brain showing scattered or extensive ischemic changes.

Urinary complaints , NPH vs BPH:

Covid19 and NPH:

In the context of Covid19, it is prudent to consider post Covid NPH. Other infections such as syphilis, cryptococcosis and Lyme disease have been associated with NPH. Possible mechanisms for NPH after COVID include disruption of choroid plexus cells by direct viral invasion or as a result of neuroinflammation and cytokine release and hypercoagulability leading to venous congestion and abnormalities of CSF flow. 

Please refer to the case report below

https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-022-07184-x

Your Checklist  ( still working on it)

It is an easy, rough assessment for you to consider 

Initial Complaint 

Gait impairement first (iNPH)---------------------------- 

Cognitive Impairement first----------------------

Incontinence/Urgency first-----------------------

Cogwheel Rigidity 

No--------------------------------------------1 

Yes (Consider Parkinson’s) -------------------------------------------0 

Resting Tremors 

No------------------------------------------1 

Yes (Consider Parkinson’s) -----------------------------------------0 

Cortical Signs (Look for Aphasia , Agnosia, Apraxia ) 

No----------------------------------------------1 

Yes---------------------------------------------0 

Radiological Examination 

Disproportionately enlarged subarachnoid space hydrocephalus (DESH)  

(crowding of the sulci superiorly near the vertex accompanied by enlargement of CSF spaces more inferiorly, particularly in the Sylvian fissures)----------1 

No-------------------------------------------------------------------------------0