70 YEAR OLD PRESENTING WITH LOSS OF SPEECH AND NECK STIFFNESS
70 YEAR OLD PRESENTING WITH LOSS OF SPEECH AND NECK STIFFNESS.
** This is an ongoing case. I am in the process of updating and editing this ELOG as and when required.
Elog made under guidance of Firdous Sameera ma'am (Intern)
Note: This is an online E Log book recorded to discuss and comprehend our patient's de-identified health data shared, AFTER taking his/her/guardian's signed informed consent.
Here, in this series of blogs, we discuss our various patients' problems through series of inputs from available global online community of experts with an aim to solve those patients' clinical problems, with collective current best evidence based inputs.
This E-log book also reflects my patient-centered online learning portfolio and of course, your valuable inputs and feedbacks are most welcome through the comments box provided at the very end.
I have been given the following case to solve, in an attempt to understand the concept of "Patient clinical analysis data" to develop my own competence in reading and comprehending clinical data, including Clinical history, Clinical findings, Investigations and come up with the most compatible diagnosis and treatment plan tailored exclusively for the patient in question.
CASE SHEET
- Loss of speech since 2 days. Patient is not sure of the exact onset, but says it has become extremely noticeable since 2 days.
- Stiffness in the neck since 2 days. Sudden onset. She reports no aggravating or relieving factors.
5 years ago patient developed weakness and giddiness and was diagnosed with hypertension.
She was prescribed TAB.ATENOLOL 25mg which she stopped 2months ago and started taking TELMA-40 as prescribed by local medical practitioner since the BP was not under control.
Also since 5yrs she developed pain in both lower limbs for which she was prescribed TAB.ACECLOFENAC AND TAB.PREDNISOLONE-5mg by an RMP and stopped taking these since the past 2months.
History of past illness:
Not a known case of diabetes, tuberculosis, bronchial asthma.
Personal history:
- She takes a mixed diet but has a decreased apetite
- Bowel movement is regular. Bladder movement is normal and regular
- She takes adequate sleep.
- No known allergies
- No relevant family history.
- TAB. ATENOLOL 5mg
- TAB. TELMA 40mg
- TAB. ACECLOFEANC
- TAB. PREDNISOLONE 5mg
Pallor: - Observed in palpebral conjunctiva and palms.
Icterus: - Not seen
Cyanosis: - Not seen
Clubbing: - Not seen
Koilonychyia: - Not seen
Lymphadenopathy: - Not seen
Edema: - Not seen
Vitals:
BP: 130/80 mmHg( After inflation of BP cuff carpopedal spasm in the hand was observed as Trousseau sign was elicited)
PR: 105 beats per minute
RR: 22 cycles per minute
Temperature: Afebrile
Systemic examination:-
- Soft and tender
- No mass and all quadrants moving equally with respiration
- No distension.
Cardiovascular system Examination :
- Cardiac sounds s1 and s2 heard normally
- No cardiac murmurs
- Thrills absent
Respiratory system examination
- Normal vesicular breath sounds heard
- No chest wall deformity
- Trachea central
- Expansion is symmetrical
- Percussion note is resonant
- No wheeze or crackles heard.
- Vocal resonance normal and symmetrical
Central nervous system Examination :
- Conscious and coherent
- Motor system reflexes normal.
- Speech: sluggish, slow response
- Signs of meningeal irritation absent
- Cranial nerves are intact
- Cogwheel rigidity is seen in that patient.
- Slow sluggish Gait. Patient appears to have difficulty in maintaining balance while walking.
- ECG:
- COMPLETE BLOOD PICTURE: Patient has normochromic normocytic anemia with a hemoglobin level of 10.1. Slight leucocytosis is also seen
- SERUM CREATININE: Patient has elevated level of serum creatinine at 2.3mg/dl
- BLOOD UREA:
- SERUM ELECTROLYTES: Within normal range.
MRI: There is a large acute infarct in left frontal lobe in ACA territory. Old infarct in right lentiform nucleus and corona radiata. Diffuse cerebral atrophy is seen. Chronic microvascular changes due to ischemia are seen. Bilateral periventricular hyperintensities have been observed.
- Xray
Diagnosis:
On the 5th day final diagnosis was made. It was found that initial provisional diagnosis of Parkinsonism was incorrect.
Patient is diagnosed with left frontal lobe infarction in ACA territory.
**EDIT dated 29th July 2021: Patient has left frontal lobe infarction resulting in arteriosclerotic Hemiparkinsonism. This article was particularly helpful in understanding this diagnosis. Click here to view article
Treatment received at the hospital:
Day 1
1. Inj OPTINEURON l amp in 100 ml N/S IV/OD.
X - 1 - X
2. Tab MIFENAC - MR PO/BD
1 - X - 1
3. Tab PAN 40 mg PO/BD
1 - X - X
4. Tab FLUPERTINE PO/BD
1 - X - 1
5. oint OMNIGEL For L/A TID
✓ - ✓ - ✓
6. Tab SHELCAL PO/OD
X - 1 - X
7. IFT Neck Intermittent T cervical fraction
8. GRBS Monitoring 12th hourly charting.
9. Tab Telma 40 mg PO/OD
10. Cervical collar
Day 2
Same treatment was continued. Following were added:
1.Tab UPRISE D3 60,000 IU weekly once
2.Tab Syndopa 110 mg BD were added.
Day 3
Same treatment was continued.
Day 4
Same treatment was continued
Day 5
Syndopa 110mg BD stopped
TAB CLOPITAB 75mg PO/OD AND
TAB ECOSPIRIN-AV 75/20mg PO/OD were added
TAB HIFENAC-MR PO/BD
TAB TELMA 40 PO/OD AND
TAB FLUPIRTINE PO/BD
Rest of the treatment was same
Day 6,7 and 8
same treatment as day 5
1.TAB CLOPITAB 75mg PO/OD
2.TAB ECOSPIRIN -AV 75/20mg PO/OD
3.INJ OPTINEURON 1amp in 100ml NS/IV/OD
4.TAB PAN 40mg PO/OD
5. oint OMNIGEL For L/A TID
✓ - ✓ - ✓
6. Tab SHELCAL PO/OD
X - 1 - X
7. Tab Uprise D3 60,000 IU Once a week
CASE DISCUSSION
This section has been included to enhance understanding of this case. I have included links to articles, presentations and PDFs that I used to clear my understanding of this case. This discussion is in the form of questions and answers. Feel free to ask questions in the comment section and I will try to update with more answers.
Q1] What is the pathology in the artery causing an infarct?
**This answer has been directly quoted from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7589849/ the article describes stroke, its pathophysiology and treatment.
A1] Stroke can be defined as an abrupt neurological outburst caused by impaired perfusion through the blood vessels to the brain. The blood flow to the brain is managed by two internal carotids anteriorly and two vertebral arteries posteriorly (the circle of Willis).
A stroke can be hemorrhagic, ischemic And transient ischemic strokes.
Ischemic stroke is caused by deficient blood and oxygen supply to the brain; hemorrhagic stroke is caused by bleeding or leaky blood vessels.
Ischemic occlusions make up around 85% of casualties in stroke patients, with the remainder due to intracerebral bleeding . In thrombosis, the blood flow is affected by narrowing of vessels due to atherosclerosis. The build-up of plaque will eventually constrict the vascular chamber and form clots, causing thrombotic stroke.
In an embolic stroke, decreased blood flow to the brain region causes an embolism; the blood flow to the brain reduces, causing severe stress and untimely cell death (necrosis). Associated pathology with stroke are inflammation, loss of homeostasis, acid-base imbalance, increased intracellular calcium levels, free radical-mediated toxicity, cytokine-mediated cytotoxicity, complement activation, impairment of the blood–brain barrier, activation of glial cells, oxidative stress and infiltration of leukocytes.
Hemorrhagic stroke accounts for approximately 10–15% of all strokes and has a high mortality rate.
In this condition, stress in the brain tissue and internal injury cause blood vessels to rupture. It produces toxic effects in the vascular system, resulting in infarction.
It is classified into intracerebral and subarachnoid hemorrhage.
In ICH, blood vessels rupture and cause abnormal accumulation of blood within the brain. The main reasons for ICH are hypertension, disrupted vasculature, excessive use of anticoagulants and thrombolytic agents.
In subarachnoid hemorrhage, blood accumulates in the subarachnoid space of the brain due to a head injury or cerebral aneurysm.
Q2] What is the pathophysiology seen in this woman? What were the risk factors involved?
A2] The pathophysiology has been highlighted above. The risk factors are best understood by dividing them into modifiable and non-modifiable risk factors. In this particular patient age(70 years), Hypertension were predisposing to a stroke.
Q3] Why was Syndopa stopped? Can these treatments not go on simultaneously?
A3] Syndopa or Levodopa are symptomatic treatments for rigidity and tremors seen in Parkinsonism. Team providing treatment to patient saw that these are not heightened in patient and she does not require this medication at the moment.
Line of treatment right now was to prevent any future infarcts thus patient has been put on antiplatelets( Clopitab and Ecospirin) her hypertension medicines are being continued as is.
Apart from this, a similar case study helped me understand the case better, do give it a read https://www.ahajournals.org/doi/10.1161/01.STR.32.1.258
To understand association of infarct with effected broca areas and manifestation in this patient in the form of loss of speech refer to this powerpoint presentation https://www.slideshare.net/drprashant24/frontal-lobe-syndromes
Read more about a typical case of frontal lobe syndrome here https://www.ncbi.nlm.nih.gov/books/NBK532981/
More on typical presentation of vascular parkinsonism here https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6327701/
Our case was of arteriosclerotic parkinsonism as a result of frontal lobe infarction. The above links will clear up doubts pertaining to the conditions as individual cases.
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