What is hemiparesis

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Hemiparesis

Definition

Hemiparesis is partial weakness (reduced motor power, but not complete loss) affecting one side of the body - typically the arm, leg, and sometimes the face on the same side. It is distinct from hemiplegia, which means complete paralysis of one side. Both result from damage to the upper motor neuron (corticospinal/corticobulbar) pathways.

Anatomy and Localization

The weakness pattern depends on exactly where the corticospinal tract is damaged:

Lesion Location	Side of Weakness	Features
Motor cortex or medulla (above pyramidal decussation)	Contralateral	May spare leg (watershed) or face
Cervical spinal cord (below decussation)	Ipsilateral	Brown-Sequard if hemicord
Posterior limb of internal capsule	Contralateral	Often "pure motor" - no sensory loss
Ventral pons / basis pontis	Contralateral	Often with dysarthria, dysphagia
Cerebral peduncle	Contralateral	May involve CN III (Weber syndrome)
Medullary pyramid	Contralateral	May involve CN XII

The upper motor neuron signs are almost always present: increased tone, hyperreflexia, and a Babinski sign (extensor plantar response).

Types of Hemiparesis

1. Pure Motor Hemiparesis

Weakness of the face, arm, and leg on one side with no sensory loss, no aphasia, no neglect, no visual deficits. The most common cause is a lacunar infarction (small deep infarct) of the:

Posterior limb of the internal capsule
Basis pontis (ventral pons)
Cerebral peduncle
Medullary pyramid

It is often accompanied by dysarthria ("dysarthria-hemiparesis" syndrome).

2. Hemiparesis Sparing the Face

Weakness of the arm and leg without facial involvement - suggests the lesion is above the facial motor cortex level (e.g., watershed infarct in the anterior cerebral-middle cerebral territory, or a lesion of the posterior limb of the internal capsule far from the genu). This includes the classic "man in the barrel" syndrome where proximal muscles are more affected than distal.

3. Ataxic Hemiparesis

A lacunar syndrome where hemiparesis (worse in the lower limb) is combined with ipsilateral cerebellar-type ataxia. The lesion is typically in the contralateral basis pontis at the junction of the upper one-third and lower two-thirds.

4. Dysarthria-Clumsy Hand Syndrome

A related lacunar syndrome: facial weakness + severe dysarthria + hand clumsiness with mild paresis. Caused by vascular lesions at the same pontine junction or in the genu of the internal capsule.

Common Causes

Stroke (most common) - ischemic infarct, hemorrhage
- Lacunar infarction (pure motor hemiparesis)
- Middle cerebral artery territory infarct (face + arm > leg)
- Anterior cerebral artery territory infarct (leg > arm)
Multiple sclerosis - a demyelinating plaque in the internal capsule or pons can mimic lacunar stroke, especially in young patients; symptoms typically worsen with heat (Uhthoff's phenomenon)
Brain tumor or abscess - mass lesion compressing or infiltrating motor pathways
Trauma - contusion or hemorrhage
Cerebral abscess
Intracranial hemorrhage - hypertensive bleeds commonly in the internal capsule or putamen

Clinical Features and Signs

Upper motor neuron findings on the affected side:

Muscle weakness (partial, graded 1-4/5 on MRC scale)
Increased muscle tone (spasticity - velocity-dependent)
Hyperreflexia (brisk or clonus)
Positive Babinski sign (extensor plantar response)
Pronator drift (on arm outstretching test)
Decreased arm swing on the affected side when walking
Circumduction gait - the affected leg swings outward in an arc
Dysarthria if corticobulbar tract involved
Possible aphasia (dominant hemisphere lesion) or hemineglect (non-dominant hemisphere lesion) if the cortex is also involved

Key Distinction: UMN vs. LMN Hemiparesis

Hemiparesis is almost always an upper motor neuron (UMN) pattern:

Feature	UMN (Hemiparesis)	LMN
Tone	Increased (spastic)	Decreased (flaccid)
Reflexes	Hyperreflexia	Hyporeflexia/absent
Babinski	Present	Absent
Atrophy	Mild (disuse)	Prominent
Fasciculations	Absent	May be present

Diagnosis

MRI brain - gold standard; detects infarcts, demyelination, hemorrhage, tumors
CT brain - fast; detects hemorrhage acutely
MR angiography / CT angiography - to assess vessel patency
CSF analysis - for demyelination (oligoclonal bands), infection
Vascular risk factor screen - blood pressure, glucose, lipids, ECG

Management (General Principles)

Treat the underlying cause (e.g., thrombolysis/thrombectomy for acute ischemic stroke, neurosurgery for hemorrhage or tumor)
Early physiotherapy and rehabilitation to maximize motor recovery
Occupational therapy for ADL adaptation
Spasticity management: physiotherapy, baclofen, tizanidine, botulinum toxin injections
Secondary prevention (antiplatelet agents, anticoagulation for cardioembolic causes, BP/lipid control)

Sources: Neuroanatomy through Clinical Cases, 3rd Edition; Localization in Clinical Neurology, 8th Edition

Need assistance in everything and on liquid diet and fumbling while talking Give chief compliance in patients language

Chief Complaint (in patient's own words):

"I can't do anything on my own — I need help with everything. I can only swallow liquids, and my speech has become unclear and slurred."

Formal Chief Complaint (clinician documentation):

Patient presents with inability to perform activities of daily living independently, dysphagia limited to liquid diet, and dysarthria (slurring/fumbling of speech).

Clinical interpretation of these three complaints together:

Patient's Words	Medical Term	Significance in Hemiparesis
"Need help with everything"	Functional dependence / hemiparesis	Weakness of one side affecting self-care, mobility, dressing, feeding
"Only on liquids"	Dysphagia (oropharyngeal)	Corticobulbar tract involvement - impaired swallowing muscles
"Fumbling while talking"	Dysarthria	Corticobulbar tract involvement - impaired articulation muscles

Taken together, dysphagia + dysarthria + functional dependence from limb weakness points strongly to corticobulbar and corticospinal tract involvement - classic for a lesion in the internal capsule or basis pontis (e.g., lacunar infarction, stroke, or demyelination).

This triad warrants urgent neurological assessment, MRI brain, and a formal swallowing evaluation (speech and language therapy referral) to prevent aspiration.

+14 more

Ramesh V chandramore 71 yrs male went to take groceries felt down road soo neighbours took to nashik civil hospital no facility avl soo patients relative decided to shift to KEM soo ca,e to Kem Emergency medicine department give present medical history

analyse_media

Here is the Present Medical History compiled from all the documents in standard clinical format:

PRESENT MEDICAL HISTORY

Mr. Ramesh Waman Chandramore | Male | 71 Years 2 Months

Chief Complaint (in Patient's Language)

"Mala chakkar aala, mi padloh, mala kळt nahi kahaan aahe, bolayala traas hoto" (I felt dizzy, I fell down, I was confused about where I was, and I had difficulty speaking)

History of Present Illness

Mr. Ramesh Waman Chandramore, a 71-year-old retired municipal employee, was apparently well until 06-Jul-2026 at approximately 12:00 - 12:30 PM, when he suddenly felt giddy and fell down while going to purchase groceries in Nashik. He was found on the road by neighbours.

Following the fall, he was noted to be:

Unconscious / disoriented - unable to identify where he was
Slurring of speech (dysarthria) - fumbling/unclear words
Unable to perform activities independently (functional dependence)

He was first taken to Nashik Civil Hospital, where adequate facilities were not available. His relatives then decided to transfer him to KEM Hospital, Mumbai. He was brought to the KEM Emergency (Casualty) Department by his wife, Hira Chandramore, along with a pink slip referral from Nashik due to disorientation.

He arrived at KEM Casualty at 08:13 on 06-Jul-2026 and was subsequently shifted to the EMS unit at 00:52 (midnight).

Sequence of Events (Timeline)

Time	Event
~12:00-12:30 PM, 06-Jul-2026	Sudden giddiness → fall on road in Nashik
Shortly after	Disorientation noted; neighbours took him to Nashik Civil Hospital
No facility available	Relatives decided to transfer to KEM, Mumbai
06-Jul-2026, 08:13 AM	Arrived at KEM Casualty with wife; referred with pink slip
06-Jul-2026, 00:52 AM (next day)	Admitted to Ward 9 (General Medicine), EMS Unit

On Examination at KEM (EMS Notes)

General Condition: Poor
Conscious: Yes, but Disoriented
BP: 130/80 mmHg
SpO2: 99%
Heart Rate: 84/min
Height/Weight: 230 (likely weight in context)
CVS: S1 S4 heard (S4 suggests reduced ventricular compliance - hypertensive/ischemic)
CNS: Conscious, disoriented; Power could not be assessed (due to altered sensorium)
Plantar: Right - Upgoing (Babinski positive - UMN sign)
Respiratory: AEBE (Air Entry Bilaterally Equal)
Blood Glucose (HGT): Not documented but insulin sliding scale ordered (if HGT >180)
GCS recorded on ward: E4 V4 M6 = GCS 14/15

Investigations Done

1. CT Brain (Plain + Angiography) - 06-Jul-2026:

Finding	Description
Acute/Subacute lesion	Ill-defined hypodensity with loss of grey-white matter differentiation in left corona radiata - subacute non-hemorrhagic infarct
Old lesion	Chronic lacunar infarct in right corona radiata
Background changes	Age-appropriate cerebral atrophy; periventricular hypodensities (chronic ischemic changes) bilaterally
Hemorrhage	No evidence of acute hemorrhage
Brainstem/Cerebellum	Normal
Vessels (Angio)	Atherocalcific changes in bilateral carotid bulbs (20-30% narrowing); bilateral ICA cavernous segment (30-40% narrowing); clinoid/supraclinoid bilateral ICA (30-40% right, 20-30% left). MCA, ACA, PCA, vertebrals all normal. No leptomeningeal enhancement.

2. HbA1c - 07-Jul-2026: 5.90 gm% (Pre-diabetic range: 5.7-6.4) | Mean Plasma Glucose: 132.7 mg/dL

3. USG Abdomen - 06-Jul-2026:

Liver: RLS 12.9 cm, mildly altered echotexture (correlate with LFT) - no focal lesion
Gallbladder: Partly distended
Left kidney: Exophytic cortical cyst 4 x 3.5 cm at upper pole
Impression: No significant abnormality

Treatment Initiated (EMS/Ward)

Drug	Purpose
Inj. Mannitol 100 cc BD	Cerebral edema reduction
IVF NS + MVI	Hydration + multivitamins
Tab Aspirin 150 mg OD	Antiplatelet
Tab Clopidogrel 75 mg HS	Antiplatelet (dual)
Tab Atorvastatin 40 mg OD	Statin - plaque stabilization
Tab Amlodipine 10 mg OD	Antihypertensive
Inj. Pantoprazole 40 mg OD	Gastric protection
Inj. Thiamine 100 mg in NS	Neuroprotection / Wernicke's prophylaxis
Inj. Ceftriaxone 1g BD	Antibiotic (infection prophylaxis)
Inj. Metronidazole 100 ml TDS	Antibiotic coverage
Insulin sliding scale (if HGT >180)	Glycaemic control
T. MVBC BD	Vitamin B complex
T. Amlo 10 OD	Antihypertensive

Summary (Clinical Impression)

Mr. Ramesh Chandramore, a 71-year-old male with background atherosclerotic cerebrovascular disease, presented with sudden onset giddiness, fall, disorientation, and slurring of speech consistent with an acute ischemic stroke (subacute non-hemorrhagic infarct, left corona radiata) superimposed on a chronic right-sided lacunar infarct - likely explaining a right-sided hemiparesis/UMN pattern (right Babinski positive on exam, functional dependence, dysarthria). He is now admitted under General Medicine - EMS Unit, on dual antiplatelet therapy, statin, antihypertensives, and physiotherapy.These are the same CT Brain (Plain + Angiography) report images already analysed in the previous response. Here is a focused breakdown of the CT findings for Mr. Ramesh Waman Chandramore:

CT BRAIN (Plain + Angiography) Report

KEM Hospital, Dept. of Radiology | Date: 06-Jul-2026 | CT No: CT662970 Reported by: Dr. Padma V Badhe (MD Radiology) | Dr. Jai Rajesh Rathi

History (as sent for CT)

"C/O slurring of speech following giddiness and fall"

NCCT Brain Findings

Finding	Details
Acute / Subacute lesion	Ill-defined hypodensity with loss of grey-white matter differentiation in left corona radiata - suggestive of subacute non-hemorrhagic infarct
Old / Chronic lesion	Chronic lacunar infarct in right corona radiata
Cerebral atrophy	Generalised cerebral atrophy - opening up of sulcal spaces
Chronic ischemic changes	Periventricular hypodensities bilaterally
Brainstem & Cerebellum	Normal
Basal cisterns	No abnormality
Ventricular system	Normal
Calvarium	Normal
Hemorrhage	No evidence of acute hemorrhage

CT Angiography (Brain Angio) Findings

Vessel	Finding
Bilateral carotid bulbs	Atherocalcific wall calcifications → 20-30% luminal narrowing
Bilateral ICA (cavernous segment)	30-40% luminal narrowing bilaterally
Bilateral ICA (clinoid & supraclinoid)	30-40% narrowing on right; 20-30% on left
Left MCA & branches	Normal
Left ACA	Normal
Right MCA & branches	Normal
Right ACA	Normal
ACOM	Normal
Both vertebral arteries	Normal
Both PCAs	Normal
Dural venous sinuses	Normal opacification
Leptomeningeal enhancement	None

IMPRESSION (Official)

Subacute non-hemorrhagic infarct - left corona radiata (new/recent stroke)
Chronic lacunar infarct - right corona radiata (old stroke)
Age-appropriate cerebral atrophy with chronic ischemic changes
Atherosclerotic changes as described above

Clinical Correlation

CT Finding	Clinical Meaning
Left corona radiata infarct	Explains right-sided hemiparesis + dysarthria (corticospinal/corticobulbar tract involvement)
Right corona radiata old lacune	Evidence of prior silent/old stroke - longstanding cerebrovascular disease
Bilateral ICA narrowing (30-40%)	Underlying atherosclerotic large vessel disease - stroke mechanism likely small vessel + large vessel disease
No hemorrhage	Confirms ischemic stroke - antiplatelet therapy is safe and appropriate
Periventricular changes + atrophy	Chronic hypertensive/ischemic brain damage over years

1000013523.jpg

With uses

Here is the complete prescription from Mr. Ramesh's IPD case paper with the use/purpose of each drug explained in the context of his acute ischemic stroke:

PRESCRIPTION WITH USES

Mr. Ramesh Waman Chandramore | Ward 9, KEM Hospital | 06-Jul-2026

Monitoring Orders

#	Order	Use in This Patient
1	TPR / BP / IOC (TDS)	Monitor Temperature, Pulse, Respiration and Blood Pressure 3x/day - watch for hypertensive spikes or post-stroke autonomic instability
2	Monitor HGT (TDS)	Monitor blood glucose (HGT = HemoglucoTest) 3x/day - hyperglycemia worsens stroke outcome
3	Strict IOC (4 hourly)	Strict Intake-Output Chart every 4 hours - fluid balance monitoring, prevent over/under hydration

IV Fluids & Vitamins

#	Drug	Dose/Freq	Use in This Patient
4	Inj. Mannitol 100 cc	BD (modified from TDS)	Osmotic diuretic - reduces cerebral edema around the infarct zone; lowers raised intracranial pressure
5	IVF NS + 2cc MVI	TDS	Normal saline for IV hydration (patient on liquid diet, dysphagia); MVI = Multivitamin Injection for nutritional support

GI Protection & Anti-emetics

#	Drug	Dose/Freq	Use in This Patient
6	Inj. Pantoprazole (PAN) 40 mg	OD	Proton pump inhibitor - gastric protection against stress ulcers (common in acute stroke/ICU patients) and from aspirin use
7	Inj. Ondansetron (EMSET) 4 mg	BD	Anti-emetic - controls nausea and vomiting associated with acute stroke and raised ICP (from Mannitol use period)

Antiplatelet & Statin (Stroke Core Treatment)

#	Drug	Dose/Freq	Use in This Patient
8	Tab Aspirin 150 mg	OD	Antiplatelet agent - prevents further clot formation in cerebral vessels; standard therapy in acute ischemic stroke
9	Tab Atorvastatin (ATORVAS) 40 mg	OD (night)	High-intensity statin - stabilises atherosclerotic plaques in bilateral ICA (as seen on CT angio), reduces LDL, prevents recurrent stroke
10	Tab Clopidogrel (CLOPI) 75 mg	HS (night)	Antiplatelet - used with aspirin as dual antiplatelet therapy (DAPT) in acute ischemic stroke - reduces risk of early stroke recurrence

Antihypertensive

#	Drug	Dose/Freq	Use in This Patient
12	Tab Amlodipine (AMLO) 10 mg	OD	Calcium channel blocker - controls hypertension; BP was 130/80 on admission - long-term BP control reduces recurrent stroke risk

Neuroprotection / Vitamins

#	Drug	Dose/Freq	Use in This Patient
11	Inj. Thiamine 100 mg in 1 pint NS	OD (modified)	Vitamin B1 - neuroprotection; prevents Wernicke's encephalopathy especially in elderly patients with poor oral intake; also important if alcohol use is a possibility
13	Tab MVBC	BD	Vitamin B complex (B1, B6, B12) - nerve repair support, reduces homocysteine (a stroke risk factor), nutritional supplement

Glycaemic Control

#	Drug	Dose/Freq	Use
14	Inj. HIR (Insulin Regular) - Sliding Scale (if HGT > 180 mg/dL)	TDS	Controls hyperglycemia - high blood sugar worsens brain ischemia and increases infarct size; HbA1c was 5.9 (pre-diabetic range)

Handwritten Additions

Drug	Dose/Freq	Use in This Patient
Inj. Ceftriaxone (XONE) 1g	BD	Broad-spectrum cephalosporin antibiotic - aspiration pneumonia prophylaxis / treatment (high risk due to dysphagia on liquid diet)
Inj. Metronidazole (METRO) 100 ml	TDS	Antibiotic covering anaerobes - used with ceftriaxone for aspiration pneumonia coverage (anaerobes common in aspiration)
Syp Cremaffin Plus 15 ml	HS (night)	Laxative / stool softener - prevents constipation (common in bedridden stroke patients, immobility + liquid diet)

Observations / Advise (Handwritten)

Note	Meaning
S/B SR Meds / Dr. Mahesh Sir	Seen by Senior Resident Medicine under Dr. Mahesh
E4 V4 M6 = GCS 14	Glasgow Coma Scale - patient conscious but slightly impaired verbal response
Anti-ischemic measures	Head end elevation 30°, avoid hypotension, maintain SpO2 >94%, glycaemic control
Limb OT / PT	Occupational Therapy + Physiotherapy for limb rehabilitation (right-sided hemiparesis)
CT Brain	CT Brain ordered to confirm stroke diagnosis
Plan D	Plan D = Dietician referral (for liquid diet management in dysphagia)

Summary: Why These Drugs Together?

ACUTE ISCHEMIC STROKE (Left Corona Radiata Infarct)
├── STOP further clotting     → Aspirin + Clopidogrel (DAPT)
├── STABILISE plaques         → Atorvastatin 40 mg
├── REDUCE brain swelling     → Mannitol 100 cc BD
├── CONTROL BP                → Amlodipine 10 mg
├── PREVENT aspiration infxn  → Ceftriaxone + Metronidazole
├── PROTECT stomach           → Pantoprazole
├── CONTROL nausea/vomiting   → Ondansetron
├── NOURISH + B vitamins      → Thiamine, MVBC, MVI in NS
├── MONITOR glucose           → HGT TDS + Insulin sliding scale
├── PREVENT constipation      → Cremaffin Plus
└── REHABILITATE              → Physiotherapy + OT

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