The doctors reply was outstanding and flawless. I will go through few concepts only.

The CT scan showed left basal ganglia hemorrhage (mainly putamen and globus pallidus). The location is very typical for hypertensive bleeds (deep brain structures, affecting small vessels). Other common locations are thalamus, brain stem (pons), and cerebellum. Although not very common, hypertensive lobar hemorrhages can happen as well. This is further supported by pre-existing history of hypertension. In the exams, they might ask about the mechanism behind hypertensibe bleeds, which is referred as lipohyalinosis and true arteriolar dissections (Charcot-Bouchard aneurysms).

The acute management rely first in securing ABCs. After that gradually lowering BP with IV meds as soon as possible is mandatory, not more than 2 hours from ICH onset. It is reasonable to lower BP to target within 1 hour from starting the medications. This is important to decrease the hemorrhagic expansion (HE) and was shown to improve functional outcomes. The target as per AHA/ASA guidelines is SBP of 140 with a range of 130-150. A SBP lower than 130 did not show significant benefit and was actually associated with complications/poor outcomes and harm, such as AKI, which in turn was also associated with poor outcomes. Common options are labetalol and nicardipine.

A patient with ICH should be monitored in ICU setting with frequent Neurovitals monitoring, at least for the first 24-48 hours, to detect any deterioration that could reflect HE and to closely monitor BP.

Neurosurgery consultation is a must for the consideration of surgical evacuation although this patient is not a great candidate since he is stable with good GCS with no IVH or frank midline shift. Other important things to consider is EVD insertion in the presence of hydrocephalus.

Further work up can include CTA to look for possible macrovascular etiology of the bleed and MRI to look for microangiopathic changes that can support the diagnosis, although the latest guidelines does not support over-investigating such patients (>45y, history of hypertension, typical location). Other utility for the CTA is the prediction of HE by the presence of Spot sign.

Repeating the brain CT after 24 hours (earlier if clinical worsening) is a must.

Chemical DVT prophylaxis can be started 48 hours after the ICH onset, with pneumatic compression before that. GI prophylaxis should be started from admission.

An on-call case 📟

Always Look carefully into the case details and never get carried away by one diagnosis. Diseases can resemble each other, and the patient is allowed to have more than one condition.

Above is a a practical lesson I learned from an interesting case I saw more than 6 months ago, but I can recall vividly its details.

She was a young woman in her early 20s, past medical history remarkable for morbid obesity, had a bariatric surgery about several weeks ago. Now, she came with 1-2 weeks history of progressive diplopia and difficulty walking, until she was not able to walk unassisted when she came to the hospital. She reported non-specific numbness in her feet ascending to her legs. Otherwise she denied other Neurological deficits. No history of systemic symptoms including fever, but she had one simple URTI ~3weeks ago. She does not take any medications apart from her vitamins and her family history is not revealing.

On examination, she had complete bilateral ophthalmoplegia, patchy sensory loss to pinprick in the lower limbs not following any anatomical rules without sensory level, and areflexia in the lower limbs. She cannot stand alone (will fall), but cerebellar exam was ok.

Also, during examination, we noted significant fluctuation in HR, reaching 140, then normalizes after a while, and she was comfortable.

Now, What comes to your mind? Think before scrolling down.

---------------------------------

We all thought after discussing with ER doctor even before examining the patient, that this could be miller fisher variant GBS given the recent surgery and URTI, progression over 1-2 weeks, and having the tried (ataxia, ophthalmoplegia, and areflexia). Additionally, the fluctuating HR makes a good argument that this is the autonomic dysfunction associated with GBS.

There was small detail that was not mentioned above to keep things interesting, which is the fact that she had some episodes of vomiting for which she had difficulty taking her supplements, seen by GS 1 week prior with repeated abdomen CT which was ok. Therefore, we entertained the idea of B1 deficiency since it is treatable, with devastating outcome if missed. Furthermore, B1 deficiency can present similarly, with opthlamoplegia, ataxia, and peripheral Neuropathy, and she had the risk factors (recent surgery, vomiting, non-compliance to the vitamins)

Patient was started on IVIG and Thiamine therapy.

Her NCS/EMG repeated twice and was normal, and brain/whole spine MRI was normal, with normal CSF, making GBS unlikely. This leaves B1 deficiency as the most likely diagnosis, successfully treated with excellent outcome. Unfortunately we could not take the B1 level until later after already given to the patient. She improved 100% after only few days, and was discharged later.

Although it may seem obvious to you here, such cases (even simpler ones) can fool anyone in the acute setting, especially if the doctor becomes biased to one direction/ddx (clinical Neurology is far more complex).

Basic Algorithm for the work up needed in patients with ischemic stroke. You can see the class of recommendation based on the available evidence between brackets for each suggestion. Adopted from the latest guidelines from ASA/AHA.

Congratulations to the doctors who got accepted in the Saudi board of Neurology program today. An exciting journey is Ahead of you, good luck! 🧠🤍

Cerebral small vessel disease (CSVD) is one of the most common conditions you will encounter practicing Neurology. It is a well established risk factor for ischemic strokes, ICH, cognitive decline and dementia. This is a nice summary reviewing the radiological characteristic of CSVD, which are six, but the sixth one (brain atrophy) is not shown.

Adopted from Anjail Sharrief's article about CSVD, continuum cerebrovascular disease issue 2023.

A practical algorithm for the diagnosis and management of cerebral venous thrombosis, adopted from the latest AHA scientific statement.

The picture shows multiple typical radiological CT findings of various CVT types. Which one of them indicate straight sinus thrombosis?

Good day,
The following case I saw in the past 2 weeks while covering the consultation service, hopefully you will enjoy reading through it.

This is a young male in his early 20s, with past medical history remarkable for ESRD 4 years ago on hemodialysis, secondary to membranous nephropathy.

He presented with ER with status epileptics requiring third line and intubation.

It is worth mentioning that couple of months ago he had pericarditis/myocarditis with subsequent cardiac tamponade requiring percardiocentesis ( Etiology ? Viral vs uremic). He completely recovered.

The history does not go further than this. Family reports hearing him making strange voices in the bathroom, walked on him and found him seizing (no clear semiology provided), with some episodes of confusion/agitation in between. No history of fever/constitutional symptoms, headaches, high risk behavior/recent travel, connective tissue diseases stigmata, or drug abuse. No history suggestive of focal Neurological deficits (other than his seizure), and no History of previous seizures or epilepsy risk factors.

I was called while the patient already intubated/sedated. His exam does not say much due to the heavy sedation with GCS of 3/15. The good news is that he has reactive pupils. Vitally he is hypertensive with most reading >170 SBP.

His basic labs showed elevated inflammatory markers but otherwise unrevealing.

Imagine you are the consulted doctor in this case. What is your differential so far? What are going to recommend for this patient to the other team who consulted you?


---------------------------------


The differential is wide at this point, but first things first. Patient was loaded and started with anti seizure medication (levetiractam). A STAT doses of anti-meningeal coverage given, entertaining the idea of possible CNS infection. Patient was pushed for brain CT to rule out structural etiologies, and Lumber puncture was done.

Brain CT showed non-specific scattered hypodensities and CSF analysis revealed high protein (1.4) but otherwise clean. EEG showed non-specific encephalopathy.

At this point it is less likely to be CNS infection given the isolated rise in protein only, and brain CT did not show specific findings. One of the good differentials by this point is PRES, given the clinical presentation, very high BP, and elevated protein in CSF in isolation. To be frank, I had a lot of doubts and I was not convinced (but the MRI did the job). My reasons were the significant elevation of protein in the CSF, the elevated inflammatory markers, and the recent cardiac event which could be related (? Autoimmune، ? Encephalitis), so I went unnecessarily outside the box. MRI was done later and showed multiple hyper intensities in finger like shape scattered in supratentorial and infratentorial region without diffusion restriction or contrast enhancement, representing vasogenic edema which is typical findings in PRES. (image shown).

Fortunately, BP lowered gradually and patient extubated in few days with retuning to his baseline in a week with no more seizures. From Neurology side, this is a symptomatic seizure and we usually wean off/stop the medications after 6 months if no recurrence, as opposed to 2 years in case of epilepsy.

A couple of lessons we can learn here:
- PRES can have high protein in CSF, it was evident in multiple studies and proportional to the degree of involvement in brain imaging.
- Patients with renal disease have particularly higher risk of developing PRES.
- Extreme high BP is the one of the common triggers, but other triggers such as certain medications exist.
- The main mechanism is a failure of auto-regulatory mechanisms in the brain, but others exist such as endothelial dysfunction.
- The main management is controlling the trigger, and the condition is typically reversible.

Please feel free to share your thoughts/questions in the private chat (new tool in the channel).

Any abnormal movement is frequently confused as seizure by many colleagues in the hospital. It is very common as Neurology practitioner to be called in the hospital or even ICU to see a patient with repetitive movement, asking you if it is a seizure, with subsequent decision regarding the need for initiation of anti-seizure medications.

So what are the features that favor seizures over other differential?
1. Rhythmic
2. Associated alteration in vital signs during the event.
3. Unreactive pupils during the event.
4. Not suppressible (you cannot stop it with your hands).
5. Upgoing planter response is also concerning for on-going seizure activity.

However, do not put a lot of weight in your decision on these individual signs, as the overall clinical picture should be taken into account.

An example of suppressible movement can be seen in the video attached.

Describe what you see.

In the beginning, you can see a cluster of an electrical like, rapid jerks lasting a fraction of a second, which looked generalized, representing myoclonus. It was then followed by extensor posturing of the upper limbs, representing the tonic phase, associated with uprolling of the eyes and unresponsiveness. This was shortly followed by generalized rhythmic jerks as well, indicating clonic phase of the event. All of this lasted around ~90 seconds, followed by sleepiness and hypo-activity.

So this patient had clusters of generalized myoclonic jerks with evolution eventually to generalized tonic-clonic seizure. The patient is known to have generalized epilepsy.

The video was taken from Bradley and Daroff's text book.

The following is a nice case seen in general Neurology rounds.

This is a man in his early 50s with unremarkable past medical history presented with transient episode of confusion lasted around 3 hours. He is back to his baseline upon evaluating him in ER.

He went to pray and afterwards he started to forget recent things such as praying, seeing somebody, or basically anything that happened recently in the past. For example, he prayed the same prayer 5 times (thinking that he never prayed each time). His wife mentioned that he still knows them and remembers his identity. Patient remembers that 3 hours as a hazy period, not very clear. He reported very poor sleep and high work stress over the past 1 week.

Denied any fever, constitutional symptoms, headache, connective tissue disease stigmata, or any other Neurological symptoms. No seizures/myoclonus.

Neurological and cognitive exams are normal. He is back to his baseline now.

Basic labs are ok. CSF analysis is normal. EEG is normal.

Brain MRI (DWI and ADC) is shown. Review the imaging before scrolling down to the rest of the case.

Can you spot the diagnosis?


--------------------------------


MRI brain showed tiny dot of diffusion restriction in the left lateral hippocampus.

These MRI findings along with transient nature of his memory loss (anterograde and recent events) are typical for transient global amnesia.

The condition is benign and as the name suggests transient. The pathophysiology still not well established, with theories including vascular, migrainous, and epileptic. It commonly follows a trigger such as intense stress or physical activity, among others.

A Women in her 60s brought with History of rapidly progressive cognitive decline within few months, visual/auditory hallucinations, myoclonus, and ataxia.

What do you see in the brain MRI shown?
What is your top Differential diagnosis? how to confirm it?

https://youtu.be/y50LwwQ7gCM

This is a lecture I presented couple of days ago about nystagmus. I hope you find it useful.

All thanks to Saudi Neurology interest club for the invitation and excellent organization. 🙏🏼🧠

A summary of paraneoplastic Neurological syndromes along with their associated antibodies and primary cancers. Knowledge about these syndromes and their associated serological testing and malignancies is important for earlier detection, earlier start of immunotherapy, and appropriate cancer screening plan, which eventually can alter patient's outcome.